The polyol pathway involves the conversion of glucose to sorbitol using the enzyme aldose reductase in hyperglycemic conditions. This leads to accumulation of sorbitol which can cause osmotic and oxidative stress damage. It also depletes NADPH levels needed for other cellular processes. Increased polyol pathway activity is implicated in diabetic complications affecting the eyes, kidneys, nerves and blood vessels. Inhibiting aldose reductase may help prevent complications by reducing sorbitol levels and metabolic imbalances caused by the polyol pathway under hyperglycemic conditions.
- Fructose metabolism occurs primarily in the liver, intestine and kidney. Fructose is converted to fructose-1-phosphate by fructokinase and can then enter the glycolysis or gluconeogenesis pathways.
- Defects in fructose metabolism can cause disorders like essential fructosuria (deficiency of fructokinase) or hereditary fructose intolerance (deficiency of aldolase B). Patients with these defects need to restrict dietary fructose intake.
- The polyol pathway converts glucose to fructose via sorbitol and is related to complications of diabetes like cataracts due to sorbitol accumulation inside cells. Inhibitors
The document discusses fatty liver and the biochemical basis and clinical conditions that can cause fatty liver. It notes that accumulation of abnormal quantities of lipids (>25-30% as triglycerides) in the liver is called fatty liver infiltration. Conditions that can cause fatty liver include starvation, diabetes, obesity from excess calorie intake, alcohol abuse, toxins, drugs, protein-energy malnutrition, and certain hormones. It also discusses lipotropic factors, which are substances that help mobilize fat and prevent its accumulation in the liver, such as choline, betaine, methionine, essential fatty acids, inositol, and some vitamins and minerals. Lipotropic factors can prevent fatty liver but cannot reverse an existing condition
This document discusses the metabolism of fructose and galactose. It outlines the dietary sources and absorption pathways of each sugar. Fructose is metabolized separately in the liver and muscle, while galactose is metabolized through a pathway involving phosphorylation, reduction, and synthesis of UDP-galactose. The document also describes inborn errors that can occur in these metabolic pathways, including fructokinase deficiency, aldolase B deficiency, and classic galactosemia due to galactose-1-phosphate uridylyltransferase deficiency. These errors can result in conditions like fructosuria, fructose intolerance, and galactosemia.
Glycogen is the storage form of carbohydrates in the human body, primarily in the liver and muscle. The liver stores glycogen to provide glucose to maintain blood sugar levels during periods of starvation. Muscle stores glycogen to act as a fuel reserve for muscle contraction, becoming depleted during prolonged exercise.
GLYCOGEN STORAGE DISEASE , GSD , Von Gierke DiseaseRAHUL KATARIA
Detailed presentation about glycogen storage disease.
description about all types of GSDs like .
1. GSD I
2.GSD III
3. GSD IV
4. GSD VI
5. GSD IX
6. GSD 0
This document discusses fructose metabolism in the liver and extrahepatic tissues. It notes that fructose is metabolized to fructose-1-phosphate in the liver by fructokinase and can then enter pathways like glycolysis, glycogen synthesis, or lipogenesis. In extrahepatic tissues, fructose is first phosphorylated to fructose-6-phosphate by hexokinase and can then be converted to glucose-6-phosphate and enter glycolysis. Excessive fructose consumption can lead to hypoglycemia, hyperuricemia, and increased fatty acid and cholesterol levels due to increased flux through these metabolic pathways. Rare genetic defects like hereditary fructose int
METABOLISM OF GALACTOSE, FRUCTOSE & AMINO SUGARSYESANNA
- Lactose in milk is broken down by lactase into glucose and galactose. Galactose is metabolized mainly in the liver.
- Galactose is converted to glucose through a series of reactions involving galactokinase, galactose-1-phosphate uridylyltransferase, and UDP-glucose 4-epimerase.
- Deficiencies in enzymes involved in galactose metabolism can cause galactosemia, a serious genetic disorder if galactose is not restricted from the diet.
The uronic acid pathway, also known as the glucoronic acid pathway, is an alternative oxidative pathway for glucose that results in the synthesis of glucoronic acid, UDP-glucose, pentoses, and ascorbic acid in lower animals. The pathway includes reactions like those catalyzed by phosphoglucomutase and UDP-glucose dehydrogenase. Administration of drugs such as barbitol and chlorobutanol increases the uronic acid pathway and synthesis of glucoronate from glucose, which is required for detoxification of these drugs. Essential pentosuria is a rare genetic disorder caused by a deficiency of xylitol dehydrogenase, preventing the conversion of L-xylulose to xylitol and
- Fructose metabolism occurs primarily in the liver, intestine and kidney. Fructose is converted to fructose-1-phosphate by fructokinase and can then enter the glycolysis or gluconeogenesis pathways.
- Defects in fructose metabolism can cause disorders like essential fructosuria (deficiency of fructokinase) or hereditary fructose intolerance (deficiency of aldolase B). Patients with these defects need to restrict dietary fructose intake.
- The polyol pathway converts glucose to fructose via sorbitol and is related to complications of diabetes like cataracts due to sorbitol accumulation inside cells. Inhibitors
The document discusses fatty liver and the biochemical basis and clinical conditions that can cause fatty liver. It notes that accumulation of abnormal quantities of lipids (>25-30% as triglycerides) in the liver is called fatty liver infiltration. Conditions that can cause fatty liver include starvation, diabetes, obesity from excess calorie intake, alcohol abuse, toxins, drugs, protein-energy malnutrition, and certain hormones. It also discusses lipotropic factors, which are substances that help mobilize fat and prevent its accumulation in the liver, such as choline, betaine, methionine, essential fatty acids, inositol, and some vitamins and minerals. Lipotropic factors can prevent fatty liver but cannot reverse an existing condition
This document discusses the metabolism of fructose and galactose. It outlines the dietary sources and absorption pathways of each sugar. Fructose is metabolized separately in the liver and muscle, while galactose is metabolized through a pathway involving phosphorylation, reduction, and synthesis of UDP-galactose. The document also describes inborn errors that can occur in these metabolic pathways, including fructokinase deficiency, aldolase B deficiency, and classic galactosemia due to galactose-1-phosphate uridylyltransferase deficiency. These errors can result in conditions like fructosuria, fructose intolerance, and galactosemia.
Glycogen is the storage form of carbohydrates in the human body, primarily in the liver and muscle. The liver stores glycogen to provide glucose to maintain blood sugar levels during periods of starvation. Muscle stores glycogen to act as a fuel reserve for muscle contraction, becoming depleted during prolonged exercise.
GLYCOGEN STORAGE DISEASE , GSD , Von Gierke DiseaseRAHUL KATARIA
Detailed presentation about glycogen storage disease.
description about all types of GSDs like .
1. GSD I
2.GSD III
3. GSD IV
4. GSD VI
5. GSD IX
6. GSD 0
This document discusses fructose metabolism in the liver and extrahepatic tissues. It notes that fructose is metabolized to fructose-1-phosphate in the liver by fructokinase and can then enter pathways like glycolysis, glycogen synthesis, or lipogenesis. In extrahepatic tissues, fructose is first phosphorylated to fructose-6-phosphate by hexokinase and can then be converted to glucose-6-phosphate and enter glycolysis. Excessive fructose consumption can lead to hypoglycemia, hyperuricemia, and increased fatty acid and cholesterol levels due to increased flux through these metabolic pathways. Rare genetic defects like hereditary fructose int
METABOLISM OF GALACTOSE, FRUCTOSE & AMINO SUGARSYESANNA
- Lactose in milk is broken down by lactase into glucose and galactose. Galactose is metabolized mainly in the liver.
- Galactose is converted to glucose through a series of reactions involving galactokinase, galactose-1-phosphate uridylyltransferase, and UDP-glucose 4-epimerase.
- Deficiencies in enzymes involved in galactose metabolism can cause galactosemia, a serious genetic disorder if galactose is not restricted from the diet.
The uronic acid pathway, also known as the glucoronic acid pathway, is an alternative oxidative pathway for glucose that results in the synthesis of glucoronic acid, UDP-glucose, pentoses, and ascorbic acid in lower animals. The pathway includes reactions like those catalyzed by phosphoglucomutase and UDP-glucose dehydrogenase. Administration of drugs such as barbitol and chlorobutanol increases the uronic acid pathway and synthesis of glucoronate from glucose, which is required for detoxification of these drugs. Essential pentosuria is a rare genetic disorder caused by a deficiency of xylitol dehydrogenase, preventing the conversion of L-xylulose to xylitol and
This document discusses lipoprotein disorders and their relationship to cardiovascular disease. It begins by describing the general structure of lipoproteins, which consist of a nonpolar lipid core surrounded by amphipathic proteins and lipids. It then covers the classification of lipoproteins based on density, describes various genetic lipoprotein disorders like familial hypercholesterolemia and their effects, and discusses specific disorders involving high-density lipoproteins, triglyceride-rich lipoproteins, and lipoprotein processing enzymes. The document provides an overview of the pathogenesis and clinical manifestations of major lipoprotein disorders and their implications for cardiovascular risk.
Complete Set of Metabolism of Carbohydrate in that second chapter, glycolysis.
This presentation covers complete glycolysis pathway with step wise animated reactions and it includes clinical aspects also. This presentation is good for MBBS students.
This document discusses various disorders of lipid metabolism. It begins by describing Fredrickson's classification of hyperlipidemias. It then discusses specific disorders in more detail, including chylomicron syndrome, familial hypercholesterolemia, familial defective apoB3500, familial combined hyperlipidemia, familial hypertriglyceridemia, type III hyperlipoproteinemia, and polygenic hypercholesterolemia. For each disorder, it provides information on prevalence, genetic factors, clinical presentation, diagnostic criteria, and treatment approaches.
Fatty liver refers to excess triglyceride deposition in liver cells. The balance between factors that cause fat deposition and removal determines if fatty liver develops. Fatty liver can result from increased fat mobilization from adipose tissue, increased fatty acid synthesis in the liver, toxic liver injury, or decreased fat oxidation in the liver. Alcoholism is a common cause as alcohol is broken down into compounds that reduce fat breakdown in the liver. Without treatment, fatty liver can progress to cirrhosis as fat accumulation damages liver cells. Certain nutrients called lipotropic factors help prevent fatty liver by aiding in fat mobilization from the liver.
The glucuronic acid pathway is a quantitatively minor route of glucose metabolism. Like the pentose phosphate pathway, it provides biosynthetic precursors and inter-converts some less common sugars to ones that can be metabolized.
This document discusses uric acid metabolism and the disease gout. It begins by explaining that uric acid is produced from the breakdown of purines and is normally excreted by the kidneys. Gout occurs when uric acid crystals deposit in the joints, causing inflammation. The document then covers the pathogenesis, risk factors, clinical features including acute attacks and chronic tophi formation, diagnosis, and management of gout with medications such as colchicine, NSAIDs, corticosteroids, allopurinol, and febuxostat. The goal of treatment is to reduce uric acid levels and prevent gout flares.
Niacin, or vitamin B3, is an essential vitamin that acts as a coenzyme in many metabolic reactions related to energy production. It is synthesized from the amino acid tryptophan. Niacin deficiency causes the disease pellagra, with symptoms of dermatitis, diarrhea, and dementia. Treatment of pellagra involves niacin supplementation. Therapeutically, niacin is used to treat hypercholesterolemia and hypertriglyceridemia by lowering LDL and VLDL cholesterol levels and raising HDL levels.
Glucose transport into cells is mediated by glucose transporter (GLUT) proteins. [1] There are five main GLUT transporters that are involved in glucose transport and each has a distinct tissue distribution and function. [2] GLUT transporters use a flip-flop mechanism to transport glucose across the cell membrane according to the concentration gradient. [3] Insulin regulates glucose transport by stimulating the translocation of GLUT4 and GLUT1 transporters from intracellular vesicles to the cell membrane, increasing the influx of glucose into cells.
These are major source of energy for living organisms.
Supplying a huge array of metabolic intermediates for biosynthetic reactions.
The structural elements in cell coat or connective tissues.
Glycogen is the storage from of glucose. The metabolism of glycogen both as glycogenolysis, breakdown of glycogen, and glycogenesis, formation of glycogen along with their regulation is briefed in the slides.
Glycogen is the major storage form of glucose found mainly in the liver and skeletal muscles. It is formed from glucose through glycogenesis and broken down into glucose through glycogenolysis. These pathways are regulated by enzymes like glycogen synthase and glycogen phosphorylase in response to hormones like insulin and glucagon to maintain blood glucose levels. Deficiencies in enzymes of glycogen metabolism can result in glycogen storage diseases characterized by hypoglycemia, hepatomegaly and other symptoms.
Thiamine (vitamin B1) is a water-soluble vitamin that acts as a coenzyme in carbohydrate metabolism. It contains pyrimidine and thiazole rings connected by a methylene bridge. Thiamine is converted to its active coenzyme form, thiamine pyrophosphate (TPP), which is involved in several metabolic reactions like pyruvate dehydrogenase complex and transketolase. Deficiency of thiamine causes beriberi disease characterized by peripheral neuropathy or heart failure.
This document summarizes several glycogen storage diseases caused by deficiencies in enzymes involved in glycogen synthesis and breakdown. Key points include: glycogen storage diseases are inherited disorders characterized by abnormal glycogen deposition; deficiencies in enzymes like glucose-6-phosphatase and acid maltase can cause hypoglycemia, lactic acidosis, hyperlipidemia, and other issues; the organs and severity of symptoms vary depending on the specific enzyme deficiency.
This document summarizes gluconeogenesis, the process by which glucose is synthesized from non-carbohydrate precursors. It describes the major substrates and sites of gluconeogenesis, its importance during fasting, and how it resembles the reversed pathway of glycolysis. Key enzymes that bypass irreversible glycolysis steps are pyruvate carboxylase, phosphoenolpyruvate carboxykinase, and fructose-1,6-bisphosphatase. Gluconeogenesis is regulated by substrates, enzymes like pyruvate carboxylase, and hormones including glucagon and glucocorticoids.
Chemistry, and biochemical role, rda, vitamin dJasmineJuliet
Vitamin D - Chemistry,n Metabloism, Biosynthesis in our skin, Recommended dietary Allowance, Dietary sources of vitamin D, Deficiency symptoms of vitamin D, Hypervitaminosis of vitamin D.
Gluconeogenesis is the formation of glucose from non-carbohydrate precursors and occurs primarily in the liver and kidneys. Key substrates include lactate, glycerol, and glucogenic amino acids. The process is regulated by substrate availability and key enzymes such as pyruvate carboxylase and phosphoenolpyruvate carboxykinase. Gluconeogenesis is critical for maintaining blood glucose levels during periods of fasting or low carbohydrate intake.
Diabeticretinopathy30 3-2011-121109075116-phpapp01mah neem mah
Aldose reductase is an enzyme that catalyzes the reduction of glucose to sorbitol in the polyol pathway. Under hyperglycemic conditions seen in diabetes, increased aldose reductase activity leads to sorbitol accumulation which is implicated in diabetic complications like retinopathy. Diabetic retinopathy progresses through mild, moderate, and severe nonproliferative stages before reaching the proliferative stage where new abnormal blood vessels form that can hemorrhage. It is a leading cause of blindness and its treatment involves controlling blood sugar, laser photocoagulation, and vitrectomy.
This document summarizes the physiology of the visual cycle. It discusses that vitamin A is obtained through diet and converted to retinal in the body. Retinal binds to opsins in the photoreceptors to form visual pigments like rhodopsin. Upon exposure to light, rhodopsin undergoes changes to bleach the retinal, after which it is regenerated through a series of reactions to restore the visual cycle. The process maintains an equilibrium between bleaching and regeneration of visual pigments to facilitate continuous vision.
This document discusses lipoprotein disorders and their relationship to cardiovascular disease. It begins by describing the general structure of lipoproteins, which consist of a nonpolar lipid core surrounded by amphipathic proteins and lipids. It then covers the classification of lipoproteins based on density, describes various genetic lipoprotein disorders like familial hypercholesterolemia and their effects, and discusses specific disorders involving high-density lipoproteins, triglyceride-rich lipoproteins, and lipoprotein processing enzymes. The document provides an overview of the pathogenesis and clinical manifestations of major lipoprotein disorders and their implications for cardiovascular risk.
Complete Set of Metabolism of Carbohydrate in that second chapter, glycolysis.
This presentation covers complete glycolysis pathway with step wise animated reactions and it includes clinical aspects also. This presentation is good for MBBS students.
This document discusses various disorders of lipid metabolism. It begins by describing Fredrickson's classification of hyperlipidemias. It then discusses specific disorders in more detail, including chylomicron syndrome, familial hypercholesterolemia, familial defective apoB3500, familial combined hyperlipidemia, familial hypertriglyceridemia, type III hyperlipoproteinemia, and polygenic hypercholesterolemia. For each disorder, it provides information on prevalence, genetic factors, clinical presentation, diagnostic criteria, and treatment approaches.
Fatty liver refers to excess triglyceride deposition in liver cells. The balance between factors that cause fat deposition and removal determines if fatty liver develops. Fatty liver can result from increased fat mobilization from adipose tissue, increased fatty acid synthesis in the liver, toxic liver injury, or decreased fat oxidation in the liver. Alcoholism is a common cause as alcohol is broken down into compounds that reduce fat breakdown in the liver. Without treatment, fatty liver can progress to cirrhosis as fat accumulation damages liver cells. Certain nutrients called lipotropic factors help prevent fatty liver by aiding in fat mobilization from the liver.
The glucuronic acid pathway is a quantitatively minor route of glucose metabolism. Like the pentose phosphate pathway, it provides biosynthetic precursors and inter-converts some less common sugars to ones that can be metabolized.
This document discusses uric acid metabolism and the disease gout. It begins by explaining that uric acid is produced from the breakdown of purines and is normally excreted by the kidneys. Gout occurs when uric acid crystals deposit in the joints, causing inflammation. The document then covers the pathogenesis, risk factors, clinical features including acute attacks and chronic tophi formation, diagnosis, and management of gout with medications such as colchicine, NSAIDs, corticosteroids, allopurinol, and febuxostat. The goal of treatment is to reduce uric acid levels and prevent gout flares.
Niacin, or vitamin B3, is an essential vitamin that acts as a coenzyme in many metabolic reactions related to energy production. It is synthesized from the amino acid tryptophan. Niacin deficiency causes the disease pellagra, with symptoms of dermatitis, diarrhea, and dementia. Treatment of pellagra involves niacin supplementation. Therapeutically, niacin is used to treat hypercholesterolemia and hypertriglyceridemia by lowering LDL and VLDL cholesterol levels and raising HDL levels.
Glucose transport into cells is mediated by glucose transporter (GLUT) proteins. [1] There are five main GLUT transporters that are involved in glucose transport and each has a distinct tissue distribution and function. [2] GLUT transporters use a flip-flop mechanism to transport glucose across the cell membrane according to the concentration gradient. [3] Insulin regulates glucose transport by stimulating the translocation of GLUT4 and GLUT1 transporters from intracellular vesicles to the cell membrane, increasing the influx of glucose into cells.
These are major source of energy for living organisms.
Supplying a huge array of metabolic intermediates for biosynthetic reactions.
The structural elements in cell coat or connective tissues.
Glycogen is the storage from of glucose. The metabolism of glycogen both as glycogenolysis, breakdown of glycogen, and glycogenesis, formation of glycogen along with their regulation is briefed in the slides.
Glycogen is the major storage form of glucose found mainly in the liver and skeletal muscles. It is formed from glucose through glycogenesis and broken down into glucose through glycogenolysis. These pathways are regulated by enzymes like glycogen synthase and glycogen phosphorylase in response to hormones like insulin and glucagon to maintain blood glucose levels. Deficiencies in enzymes of glycogen metabolism can result in glycogen storage diseases characterized by hypoglycemia, hepatomegaly and other symptoms.
Thiamine (vitamin B1) is a water-soluble vitamin that acts as a coenzyme in carbohydrate metabolism. It contains pyrimidine and thiazole rings connected by a methylene bridge. Thiamine is converted to its active coenzyme form, thiamine pyrophosphate (TPP), which is involved in several metabolic reactions like pyruvate dehydrogenase complex and transketolase. Deficiency of thiamine causes beriberi disease characterized by peripheral neuropathy or heart failure.
This document summarizes several glycogen storage diseases caused by deficiencies in enzymes involved in glycogen synthesis and breakdown. Key points include: glycogen storage diseases are inherited disorders characterized by abnormal glycogen deposition; deficiencies in enzymes like glucose-6-phosphatase and acid maltase can cause hypoglycemia, lactic acidosis, hyperlipidemia, and other issues; the organs and severity of symptoms vary depending on the specific enzyme deficiency.
This document summarizes gluconeogenesis, the process by which glucose is synthesized from non-carbohydrate precursors. It describes the major substrates and sites of gluconeogenesis, its importance during fasting, and how it resembles the reversed pathway of glycolysis. Key enzymes that bypass irreversible glycolysis steps are pyruvate carboxylase, phosphoenolpyruvate carboxykinase, and fructose-1,6-bisphosphatase. Gluconeogenesis is regulated by substrates, enzymes like pyruvate carboxylase, and hormones including glucagon and glucocorticoids.
Chemistry, and biochemical role, rda, vitamin dJasmineJuliet
Vitamin D - Chemistry,n Metabloism, Biosynthesis in our skin, Recommended dietary Allowance, Dietary sources of vitamin D, Deficiency symptoms of vitamin D, Hypervitaminosis of vitamin D.
Gluconeogenesis is the formation of glucose from non-carbohydrate precursors and occurs primarily in the liver and kidneys. Key substrates include lactate, glycerol, and glucogenic amino acids. The process is regulated by substrate availability and key enzymes such as pyruvate carboxylase and phosphoenolpyruvate carboxykinase. Gluconeogenesis is critical for maintaining blood glucose levels during periods of fasting or low carbohydrate intake.
Diabeticretinopathy30 3-2011-121109075116-phpapp01mah neem mah
Aldose reductase is an enzyme that catalyzes the reduction of glucose to sorbitol in the polyol pathway. Under hyperglycemic conditions seen in diabetes, increased aldose reductase activity leads to sorbitol accumulation which is implicated in diabetic complications like retinopathy. Diabetic retinopathy progresses through mild, moderate, and severe nonproliferative stages before reaching the proliferative stage where new abnormal blood vessels form that can hemorrhage. It is a leading cause of blindness and its treatment involves controlling blood sugar, laser photocoagulation, and vitrectomy.
This document summarizes the physiology of the visual cycle. It discusses that vitamin A is obtained through diet and converted to retinal in the body. Retinal binds to opsins in the photoreceptors to form visual pigments like rhodopsin. Upon exposure to light, rhodopsin undergoes changes to bleach the retinal, after which it is regenerated through a series of reactions to restore the visual cycle. The process maintains an equilibrium between bleaching and regeneration of visual pigments to facilitate continuous vision.
Rods and cones are the two types of photoreceptors in the retina. Rods contain the photopigment rhodopsin, which absorbs blue-green light. Cones contain one of three photopigments that absorb either long, middle, or short wavelengths of light. Rods are more numerous in the periphery of the retina while cones are concentrated at the fovea. The visual system undergoes light and dark adaptation to function across varying illumination levels. Light adaptation occurs quickly as photopigments bleach and recover. Dark adaptation is slower as rods take 30 minutes to fully recover sensitivity.
The synthesis of glycogen from glucose (glycogenesis) involves multiple enzymatic steps that takes place in the cytosol. Glucose is first converted to glucose-6-phosphate by hexokinase or glucokinase in muscle and liver respectively. It is then converted to UDP-glucose which acts as the donor of glucose units. A glycogen primer, initiated by the enzyme glycogen synthase, is required to begin glycogen synthesis. Glycogen is then elongated through alpha-1,4 glycosidic linkages by glycogen synthase and branched through alpha-1,6 linkages by the branching enzyme glucosyltransferase. This leads to the formation of the branched glyc
Vitamin A and its related compounds play an essential role in visual function through their involvement in the visual cycle. Vitamin A is obtained through the diet from animal foods as retinol and plant foods as provitamin A carotenoids. Upon exposure to light, the photopigment rhodopsin in rod cells decomposes and is regenerated through a series of reactions involving retinal and related compounds derived from vitamin A. Deficiency of vitamin A can lead to xerophthalmia, beginning with night blindness and potentially progressing to corneal ulceration and blindness if left untreated.
Chronic complications of diabetes mellitusHamza AlGhamdi
Chronic complications of diabetes mellitus can affect the macrovasculature, microvasculature, eyes, kidneys, nerves, feet and skin. Macrovascular complications include coronary artery disease, stroke and peripheral vascular disease. Microvascular complications are specific to diabetes and can damage the retina, kidneys and nerves, leading to retinopathy, nephropathy and neuropathy. Other complications discussed include diabetic eye disease, kidney disease, neuropathy, foot ulcers and infections.
Diabetic foot complications are a major source of morbidity and health care costs. They result from a complex interplay of ischemia, ulceration, infection, and Charcot's joint due to diabetes-related changes. Hyperglycemia leads to nonenzymatic glycosylation of proteins and tissues, formation of advanced glycosylation end products, and accelerated atherosclerosis. This causes peripheral vascular disease, neuropathy, and foot deformities which impair sensation and blood flow, making the feet susceptible to infection, ulceration, and gangrene. Charcot's joint is a destructive foot arthropathy caused by loss of sensation from diabetic neuropathy.
GLYCOGENOLYSIS & REGULATION OF GLYCOGEN METABOLISMYESANNA
- Glycogenolysis is the degradation of glycogen stores in the liver and muscle into glucose. It is carried out by independent cytosolic enzymes.
- Glycogen phosphorylase breaks alpha-1,4 glycosidic bonds in glycogen, producing glucose-1-phosphate. A debranching enzyme then breaks alpha-1,6 bonds to fully degrade glycogen.
- Glucose-1-phosphate is converted to glucose-6-phosphate which can be further converted to glucose by glucose-6-phosphatase in the liver, releasing it into circulation. Muscle lacks this enzyme and uses its glucose-6-phosphate in glycolysis.
- Glycogen metabolism is regulated by hormones like
COMPLICATIONS OF DIABETES BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE...Prof Dr Bashir Ahmed Dar
The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels.Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.
The document discusses the complications of diabetes mellitus, including both acute and chronic complications. Acute complications involve alterations in blood sugar levels, leading to hypoglycemia or hyperglycemia events like diabetic ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome. Chronic complications affect the macrovasculature (large blood vessels) like atherosclerosis, and the microvasculature (small blood vessels) of tissues like the eyes and kidneys. Precise management of blood sugar levels can help prevent both acute and chronic complications of diabetes.
Glycogen is a branched polymer of glucose residues that serves as a storage form of glucose. It is composed mainly of α-1,4 glycosidic linkages with branches every tenth residue by α-1,6 linkages. Glycogen is found primarily in liver and muscle cells bound in granules and provides a readily available source of glucose through breakdown. Glycogen synthesis utilizes UDP-glucose and glycogenin to initiate polymer formation, while breakdown is catalyzed by phosphorylase releasing glucose-1-phosphate and other enzymes are needed to further process the glucose for energy production.
This document provides an overview of carbohydrate metabolism and associated disorders. It discusses the regulation of glycolysis and phosphofructokinase, the significance of glycolysis in meeting energy demands, and disorders associated with deficiencies in glycolysis enzymes. It also covers topics like the Rapoport-Leubering cycle, effects of altitude on hemoglobin, and the importance of gluconeogenesis during fasting.
The document discusses glycolysis and the citric acid cycle. Glycolysis involves 10 steps that break down glucose and generate a small amount of ATP without oxygen. The citric acid cycle is a series of chemical reactions in the mitochondria that further oxidizes pyruvate from glycolysis to extract more chemical energy. It involves 8 steps that produce carbon dioxide, NADH, and FADH2 to fuel the electron transport chain for oxidative phosphorylation to generate large amounts of ATP. Both pathways are tightly regulated and provide precursors for other biological processes.
1) Alcohol is absorbed in the stomach and intestine and metabolized primarily in the liver by alcohol dehydrogenase (ADH) and cytochrome P450 enzymes, converting it mainly to acetaldehyde and then acetate.
2) Some people have a mutated form of ADH that metabolizes alcohol more slowly, leading to more severe intoxication from smaller amounts of alcohol.
3) Chronic alcohol metabolism disrupts many metabolic pathways by altering the NADH/NAD+ ratio in the liver, which can cause issues like fatty liver, hypoglycemia, and lactic acidosis.
Alcohol is absorbed from the stomach and intestine and metabolized primarily in the liver. The liver enzyme alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is then further oxidized to acetate. A small amount of alcohol is eliminated through the lungs, urine, and sweat, while the majority is metabolized in the liver. The metabolism of alcohol increases the NADH/NAD+ ratio in the liver, leading to metabolic alterations like lactic acidosis, hypoglycemia, and fatty liver. Chronic alcohol use can also damage the liver and brain, potentially causing cirrhosis and neurological issues.
The document discusses glycolysis, which is the breakdown of glucose to pyruvate with production of ATP. It occurs in the cytosol of cells and can proceed with or without oxygen present. Under anaerobic conditions, pyruvate is reduced to lactate, while in aerobic conditions pyruvate enters the citric acid cycle in mitochondria to be fully oxidized to CO2 and H2O. Glycolysis is tightly regulated by feedback inhibition and is a key energy producing process, especially under low oxygen conditions like in muscle during exercise. The citric acid cycle further oxidizes acetyl-CoA produced from pyruvate to generate more ATP through oxidative phosphorylation.
Excessive alcohol consumption can cause serious health issues. It is associated with liver disorders when consumed at more than 20-30g per day. While small amounts may provide some benefits, most of the ingested ethanol is metabolized in the liver to acetaldehyde by alcohol dehydrogenase. Chronic alcohol abuse can lead to fatty liver, alcoholic hepatitis, and alcoholic cirrhosis over time as the toxic byproducts damage liver cells. It also increases risks of certain cancers and causes nutritional deficiencies. Currently, heavy drinking affects millions of Americans and accounts for over 200,000 deaths annually mainly due to liver disease and cancer.
This document provides an overview of carbohydrate metabolism. It discusses glycolysis, which converts glucose to pyruvate or lactate with ATP production. Glycolysis can occur aerobically or anaerobically. It then covers gluconeogenesis, the TCA cycle, and glycogen metabolism. It discusses the regulation and clinical significance of these pathways, along with diseases associated with defects in carbohydrate metabolism such as glycogen storage diseases and G6PD deficiency. The pentose phosphate, glucuronic acid, and alcohol metabolism pathways are also summarized.
Dr. Jakeer Hussain discusses lactic acidosis, which occurs when blood lactate levels are elevated above 5 mmol/L along with metabolic acidosis. Lactic acidosis can be type A, due to tissue hypoperfusion, or type B, which has no evidence of hypoperfusion. Common causes of lactic acidosis include shock, metformin use, mesenteric ischemia, sepsis, lung injury, and certain drugs. The presentation depends on the underlying condition, but resolving lactic acidosis generally indicates successful resuscitation in shock.
The document outlines the fates of pyruvate and the energy yields from glycolysis. It discusses:
1) Pyruvate can be reduced to lactate by lactate dehydrogenase under anaerobic conditions, oxidatively decarboxylated to acetyl-CoA by pyruvate dehydrogenase in aerobic conditions, or carboxylated to oxaloacetate.
2) Glycolysis yields 2 ATP under anaerobic conditions from the conversion of glucose to lactate, and yields 2 additional ATP under aerobic conditions when NADH is reoxidized by the electron transport chain.
3) Other monosaccharides like fructose and galactose can enter glycolysis after
Metabolism is the network of chemical reactions that take place in living cells. It performs four main functions: obtaining energy, converting nutrients into macromolecules, assembling macromolecules, and degrading macromolecules. Metabolic pathways can be catabolic, anabolic, or amphibolic. Glycolysis converts glucose into pyruvate, generating a small amount of ATP. Pyruvate then undergoes oxidative decarboxylation to form acetyl-CoA, the entry point into the citric acid cycle. Diseases can impair glycolysis through deficiencies in enzymes like pyruvate kinase or disorders that cause lactic acidosis.
This document provides an overview of carbohydrate metabolism. It begins with an introduction to carbohydrates and their classification. It then discusses specific carbohydrate metabolic pathways in more detail, including glycolysis, glycogenolysis, glycogenesis, the citric acid cycle, and the pentose phosphate pathway. It also covers topics like glycogen storage disorders, the role of these pathways in energy production, and their regulation of blood glucose levels. Clinical implications and examples are provided throughout.
This document discusses acid-base disorders caused by renal processes. It summarizes that acid-base homeostasis is critical for normal bodily functions and is maintained through respiration and the kidneys. The kidneys play a central role through reabsorbing filtered bicarbonate, excreting acid as ammonium and titratable acidity, and generating new bicarbonate. Inherited disorders can disrupt acid-base balance by affecting transporters in the proximal tubule or distal tubule. More common renal acidosis occurs in advanced chronic kidney disease due to reduced ammonia generation.
This document provides information on carbohydrate metabolism and various pathways involved including glycolysis, the citric acid cycle, and pyruvate dehydrogenase complex. It discusses:
- The key roles of glucose and glycogen in carbohydrate metabolism
- The three phases of glycolysis and production of ATP
- Conversion of pyruvate to lactate under anaerobic conditions
- Regulation of key enzymes in glycolysis
- Significance of glycolysis in various tissues and diseases
- The citric acid cycle and its importance in energy production
Carbohydrates are the sugars, starches and fibers found in fruits, grains, vegetables and milk products. Though often maligned in trendy diets, carbohydrates — one of the basic food groups — are important to a healthy diet.
Glycolysis is a universal pathway that converts glucose into pyruvate, generating ATP through a series of 10 enzyme-catalyzed reactions. Under aerobic conditions, pyruvate enters mitochondria and is further oxidized through the citric acid cycle and electron transport chain to harvest most energy. If oxygen is insufficient, pyruvate is reduced to lactate. Glycolysis is regulated by three irreversible reactions controlled by hexokinase, phosphofructokinase, and pyruvate kinase. Cholesterol synthesis begins with acetyl-CoA and involves 13 enzymatic steps producing isoprenoid units that ultimately form cholesterol through squalene and lanosterol intermediates.
The document discusses carbohydrate metabolism and its major pathways. It describes glycolysis as the breakdown of glucose to pyruvate with ATP production. The citric acid cycle (Krebs cycle) is then discussed as the oxidation of acetyl CoA to CO2, providing most of the cell's ATP. Other pathways discussed include gluconeogenesis (glucose synthesis from non-carbs), glycogenesis/glycogenolysis (glycogen formation and breakdown), and the pentose phosphate pathway for producing NADPH and other essential cell products. Disorders of carbohydrate metabolism like glycogen storage diseases and glucose-6-phosphate dehydrogenase deficiency are also mentioned.
Glycolysis is the metabolic pathway that converts glucose into pyruvate and produces a small amount of ATP. It occurs in the cytoplasm of cells and can function aerobically or anaerobically. During aerobic glycolysis, pyruvate is further oxidized to produce more ATP. During anaerobic glycolysis, pyruvate is converted to lactate, producing less ATP. The citric acid cycle is a series of chemical reactions in the mitochondria that completes the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins to produce carbon dioxide, water, and ATP through oxidative phosphorylation. It is also known as the Krebs cycle or TCA cycle. It is a key step
This document discusses cardiac biomarkers and energy metabolism in the heart. It begins by outlining the metabolic demands of the heart and how it meets most of its ATP needs through fatty acid oxidation. The major substrates that fuel heart contraction - fatty acids, carbohydrates, ketone bodies, and lactate - are described. Biomarkers of cardiac injury like cardiac troponins, CK-MB, myoglobin, and BNP are introduced. The timing and specificity of various biomarkers in detecting acute myocardial infarction is summarized. Finally, changes in heart metabolism during ischemia and the failing heart state are briefly outlined.
This document discusses nonalcoholic fatty liver disease (NAFLD), its causes and risk factors. NAFLD is caused by fat accumulation in the liver from factors other than alcohol consumption, including genetic predisposition, environmental stresses, and metabolic stresses. The main causes discussed are insulin resistance, lipid metabolism disorders, mitochondrial dysfunction, and oxidative stress. Prevention and treatment involves lifestyle changes like a healthy diet and exercise, as well as medication to treat underlying conditions and reduce liver damage.
Laboratory Assessment Of Metabolic DisordersMoustafa Rezk
This document discusses laboratory assessment of metabolic disorders, including disorders of carbohydrate, lipid, protein, mineral, and bone metabolism. It provides definitions of diabetes mellitus and criteria for diagnosis. It also discusses the role of the laboratory in diagnosing and managing diabetes, including markers of acute and chronic control. Additionally, it covers laboratory assessment of disorders of lipid, protein, mineral, and bone metabolism.
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Lesson Outcomes:
- students will be able to identify and name various types of ornamental plants commonly used in landscaping and decoration, classifying them based on their characteristics such as foliage, flowering, and growth habits. They will understand the ecological, aesthetic, and economic benefits of ornamental plants, including their roles in improving air quality, providing habitats for wildlife, and enhancing the visual appeal of environments. Additionally, students will demonstrate knowledge of the basic requirements for growing ornamental plants, ensuring they can effectively cultivate and maintain these plants in various settings.
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Business is done in many different ways across the world. How you connect with colleagues and communicate feedback constructively differs tremendously depending on where a person comes from. Drawing on the culture map from the cultural anthropologist, Erin Meyer, this class discusses how best to manage effectively across the invisible lines of culture.
How to Create a Stage or a Pipeline in Odoo 17 CRMCeline George
Using CRM module, we can manage and keep track of all new leads and opportunities in one location. It helps to manage your sales pipeline with customizable stages. In this slide let’s discuss how to create a stage or pipeline inside the CRM module in odoo 17.
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The Science of Learning: implications for modern teachingDerek Wenmoth
Keynote presentation to the Educational Leaders hui Kōkiritia Marautanga held in Auckland on 26 June 2024. Provides a high level overview of the history and development of the science of learning, and implications for the design of learning in our modern schools and classrooms.
Decolonizing Universal Design for LearningFrederic Fovet
UDL has gained in popularity over the last decade both in the K-12 and the post-secondary sectors. The usefulness of UDL to create inclusive learning experiences for the full array of diverse learners has been well documented in the literature, and there is now increasing scholarship examining the process of integrating UDL strategically across organisations. One concern, however, remains under-reported and under-researched. Much of the scholarship on UDL ironically remains while and Eurocentric. Even if UDL, as a discourse, considers the decolonization of the curriculum, it is abundantly clear that the research and advocacy related to UDL originates almost exclusively from the Global North and from a Euro-Caucasian authorship. It is argued that it is high time for the way UDL has been monopolized by Global North scholars and practitioners to be challenged. Voices discussing and framing UDL, from the Global South and Indigenous communities, must be amplified and showcased in order to rectify this glaring imbalance and contradiction.
This session represents an opportunity for the author to reflect on a volume he has just finished editing entitled Decolonizing UDL and to highlight and share insights into the key innovations, promising practices, and calls for change, originating from the Global South and Indigenous Communities, that have woven the canvas of this book. The session seeks to create a space for critical dialogue, for the challenging of existing power dynamics within the UDL scholarship, and for the emergence of transformative voices from underrepresented communities. The workshop will use the UDL principles scrupulously to engage participants in diverse ways (challenging single story approaches to the narrative that surrounds UDL implementation) , as well as offer multiple means of action and expression for them to gain ownership over the key themes and concerns of the session (by encouraging a broad range of interventions, contributions, and stances).
2. Learning outcomes
Know what polyol pathway is, how &
when it occurs
Know the pathologies that may occur
with the pathway
in relation to diabetes mellitus and
other diseases
Know how the complications could be
treated
8/1/2015 2
3. PATHWAY
Cells use glucose for energy;
however, unused glucose enters the
polyol pathway when aldose
reductase reduces it to sorbitol.
The reduction of glucose to sorbitol(a
six carbon sugar alcohol obtained by
the reduction of the aldehyde group of
glucose) is accompanied by the
oxidation of NADPH to NADP+.
8/1/2015 3
4. CONT….
Then sorbitol is oxidized to fructose by
the enzyme sorbitol
dehydrogenase(SDH)
The oxidation of sorbitol to fructose is
paralleled by the reduction of NAD+ to
NADH.
Then after the enzyme called
HEXOKINASE can return the fructose
molecule to glycolytic pathway by
phosphorylating to form FRUCTOSE-
6-PHOSPHATE.
8/1/2015 4
7. PATHOLOGY
In a hyperglycemic state,
othe affinity of aldose reductase for glucose
rises.
ocausing much sorbitol to accumulate, and
using much more NADPH.
oleaving less NADPH for other processes
of cellular metabolism.
8/1/2015 7
8. Cont….
NADPH acts to promote nitric oxide and
glutathione production.
So, its deficiency will cause glutathione
and nitric oxide deficiency.
A glutathione deficiency, congenital
or acquired, can lead to
hemolysis(because glutathione is the
protector of cell membrane from
damage its deficiency makes cell
membrane less safe) caused by
oxidative stress.
8/1/2015 8
9. Cont…
As to nitric oxide, deficiency of
NADPH results in less production of
nitric oxide which is one of the
important vasodilators in blood vessel.
8/1/2015 9
10. Polyol pathway and Diabetes
mellitus
hyperglycemia-induced polyol
pathway hyperactivity has an
important role in the etiology of late-
onset diabetic complications.
Once sorbitol has been produced, it
does not easily diffuse across cell
membranes; this intracellular
accumulation of sorbitol may be a
factor in the etiology of diabetic
complications.
8/1/2015 10
11. Cont …
Some of the complications include
neuropathy, retinopathy, nephropathy,
keratopathy, cataract-formation,
possibly infection and atherosclerosis.
The inhibition of aldose reductase
(AR), a rate-limiting enzyme of the
pathway, could become a key element
in the prevention and reversal of
diabetic complications.
8/1/2015 11
12. Diabetic neuropathy
Clinically there has been a massive
concentration of efforts on diabetic
neuropathy.
What happens during the neuropathy
is,
• increase in intracellular sorbitol levels in the
peripheral nerve.
• results in osmotic damage, and metabolic,
structural and functional abnormalities.
8/1/2015 12
13. Cont …
It is also possible that damage of the
peripheral nerve may result from
depletion of intracellular cofactors,
such as nicotinamide-adenosine
dinucleotide phosphate (NADPH).
Moreover, accumulation caused by
hyperglycemia induced polyol pathway
hyperactivity have also been
associated with the depletion of myo-
inositol.
8/1/2015 13
14. Cont …
This may in turn decrease Na+-K+
pump activity, resulting in changes in
cellular metabolism and the
membrane structure of the peripheral
nerve.
the effect of AR inhibitors on diabetic
neuropathy is mainly via the metabolic
changes due to the inhibition of the
polyol pathway activity.
8/1/2015 14
15. Polyol pathway and
atherosclerosis
It has been hypothesized that a
reduction in Na+/K+-ATPase activity is
the major pathogenic step in the
development of hypertension.
This results in the accumulation of
intracellular Na+ and ultimately leads
to significant increases in cytosolic-
free Ca2+ concentrations [Ca2+] in
vascular smooth muscle cells.
8/1/2015 15
16. Cont…
sorbitol, Na+/K+-ATPase activity and
[Ca2+] were measured using cultured
rabbit aortic smooth muscle cells.
Epalrestst (100 IlM), an AR inhibitor,
was seen to block glucose-induced
changes in sorbitol and myo-inositol
metabolism.
reducing free cytosolic Ca2+ to control level
8/1/2015 16
17. In general
Fructose metabolism has some
dangers because fructose is
metabolized differently from glucose.
Unlike fructose
Glucose can be metabolized and
converted to ATP, which is readily
“burned” for energy by the cells’
mitochondria.
Alternatively, glucose can be stored in
the liver as a carbohydrate for later
conversion to energy
8/1/2015 17
18. Cont …
Fructose on the other hand,
is more rapidly metabolized in the liver,
flooding metabolic pathways and leading to
increased triglyceride synthesis and fat
storage in the liver.
This can cause a rise in serum triglycerides,
promoting an atherogenic lipid profile and
elevating cardiovascular risk.
Increased fat storage in the liver may lead to
an increased incidence in non-alcoholic fatty
liver disease
8/1/2015 18
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