Glucose Transporters
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Glucose transporters (GLUTs) facilitate the uptake of glucose in cells. The main GLUTs are GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5. GLUT1 transports glucose in red blood cells and various tissues. GLUT2 has low affinity and transports glucose in the liver and pancreatic beta cells. GLUT3 transports glucose into brain cells with high affinity. GLUT4 mediates insulin-dependent glucose uptake in muscle and fat cells. GLUT5 transports fructose. SGluT cotransports glucose and sodium from the intestinal and renal lumens into cells.
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Presentation glucose transporters
Glucose is the main carbohydrate in blood, circulating at 65-110 mg/100 ml. It is an important fuel for muscles. Glucose enters muscles via GLUT4 glucose transporters. There are several glucose transporters with different properties - GLUT1 transports glucose in most cells, GLUT2 in liver and pancreas, GLUT3 in neurons and testes, and GLUT4 in muscles and fat which is activated by insulin. Insulin promotes glucose uptake in muscles by recruiting more GLUT4 transporters to the membrane from intracellular storage vesicles.
METABOLISM OF GALACTOSE, FRUCTOSE & AMINO SUGARS
- 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.
Metabolic changes in well feed state, starvation ,dm
Insulin and glucagon work together to maintain blood glucose levels between 3.3-6.1 mmol/L. Insulin is produced by the pancreas and facilitates glucose uptake and storage, while inhibiting gluconeogenesis. Glucagon is also produced by the pancreas and has opposing effects, stimulating gluconeogenesis and glycogenolysis to increase blood glucose. In starvation, glycogen stores are depleted after 2 days and fatty acids and ketone bodies provide energy, with gluconeogenesis enhanced after 24 days to supply glucose to vital organs.
Fructose intolerance and Clinical diagnosis
Fructose intolerance is a disorder in which a person lacks the protein needed to break down fructose. Fructose is a fruit sugar that naturally occurs in the body. Man-made fructose is used as a sweetener in many foods, including baby food and drinks.
Glucose transport
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.
disorders of Carbohydrate metabolism
The document discusses several disorders of carbohydrate metabolism including galactosemia, hereditary fructose intolerance, lactose intolerance, hypoglycemia, and diabetes mellitus. Galactosemia is caused by a deficiency of enzymes needed to break down galactose and can cause liver damage, jaundice, and intellectual disability if untreated. Hereditary fructose intolerance is caused by a lack of the aldolase B enzyme needed to break down fructose and consumption of fructose can lead to liver failure. Lactose intolerance is caused by a lack of the lactase enzyme resulting in gastrointestinal issues upon consuming dairy. Hypoglycemia and diabetes mellitus are disorders characterized by low
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Presentation glucose transporters
Glucose is the main carbohydrate in blood, circulating at 65-110 mg/100 ml. It is an important fuel for muscles. Glucose enters muscles via GLUT4 glucose transporters. There are several glucose transporters with different properties - GLUT1 transports glucose in most cells, GLUT2 in liver and pancreas, GLUT3 in neurons and testes, and GLUT4 in muscles and fat which is activated by insulin. Insulin promotes glucose uptake in muscles by recruiting more GLUT4 transporters to the membrane from intracellular storage vesicles.
METABOLISM OF GALACTOSE, FRUCTOSE & AMINO SUGARS
- 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.
Metabolic changes in well feed state, starvation ,dm
Insulin and glucagon work together to maintain blood glucose levels between 3.3-6.1 mmol/L. Insulin is produced by the pancreas and facilitates glucose uptake and storage, while inhibiting gluconeogenesis. Glucagon is also produced by the pancreas and has opposing effects, stimulating gluconeogenesis and glycogenolysis to increase blood glucose. In starvation, glycogen stores are depleted after 2 days and fatty acids and ketone bodies provide energy, with gluconeogenesis enhanced after 24 days to supply glucose to vital organs.
Fructose intolerance and Clinical diagnosis
Fructose intolerance is a disorder in which a person lacks the protein needed to break down fructose. Fructose is a fruit sugar that naturally occurs in the body. Man-made fructose is used as a sweetener in many foods, including baby food and drinks.
Glucose transport
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.
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GALACTOSE AND FRUCTOSE(2).pptx
- Galactose is obtained through the diet primarily from lactose in milk and is metabolized mainly in the liver. It is converted to glucose through a series of enzymatic reactions involving galactokinase, galactose-1-phosphate uridylyltransferase, and UDP-glucose 4-epimerase.
- Deficiencies of galactokinase or galactose-1-phosphate uridylyltransferase can cause galactosemia, leading to an accumulation of galactose and its metabolites in tissues and symptoms including liver damage, cataracts, and intellectual disability.
- Fructose obtained through the diet is converted to glucose mainly in the liver
FRUCTOSE METABOLISM
Fructose is metabolized primarily in the liver and small intestine. In the liver, fructose is converted to fructose-1-phosphate by fructokinase using ATP as energy. Fructose-1-phosphate is then cleaved by aldolase B into glyceraldehyde and dihydroxyacetone phosphate, which both enter glycolysis to generate energy. This pathway allows fructose to be rapidly metabolized and generates intermediates for glycolysis, though it requires two ATP per fructose molecule. Disorders of this pathway can cause hypoglycemia or liver failure if not treated by avoiding dietary fructose and sucrose.
Glucose Transporters.pptx
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1. The pancreas contains clusters of cells called islets of Langerhans that secrete hormones like insulin and glucagon to regulate blood glucose levels. Insulin allows cells to take in glucose from the bloodstream and lowers blood glucose levels, while glucagon has the opposite effect.
2. In diabetes, the pancreas either produces little or no insulin (type 1 diabetes) or the body develops a resistance to insulin's effects (type 2 diabetes), disrupting the body's ability to regulate blood glucose levels and maintain homeostasis. This leads to high blood glucose levels (hyperglycemia).
3. Without enough insulin to allow cells to take in glucose, the body begins to breakdown proteins and fats
Regulation of blood glucose
Blood glucose levels are normally maintained within a narrow range through the regulation of glucose entry into and removal from the bloodstream. Hormones like insulin and glucagon act in opposition to maintain glucose homeostasis, with insulin lowering blood glucose through promoting glucose uptake in cells and glucagon raising it through stimulating glucose production and release from the liver. A variety of tissues, including muscle, adipose, liver, and brain, play roles in glucose regulation through uptake, storage, production, and utilization of glucose.
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There are 13 glucose transporter proteins (GLUTs) that transport glucose across cell membranes. They are divided into 3 classes. Class I includes GLUT1-4, the most well studied of which are GLUT1, GLUT2, GLUT3 and GLUT4. GLUT1 transports glucose across the blood-brain barrier. GLUT2 acts as a bidirectional transporter in the liver and pancreas. GLUT3 transports glucose into neurons. GLUT4 is the insulin-regulated transporter that transports glucose into muscle and fat cells for storage. Defects in these transporters can lead to diseases like diabetes.
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Galactosemia is a rare genetic disorder caused by a deficiency of the enzyme galactose-1-phosphate uridylyl transferase (GALT). This enzyme is needed to break down the sugar galactose. Without it, galactose builds up and causes serious health issues. The disorder is inherited in an autosomal recessive pattern and affects how the body processes lactose from milk. Symptoms in infants can include vomiting, jaundice, and failure to thrive if not treated early through a strict lactose-free diet. While not curable, dietary management throughout life can prevent complications and allow those with galactosemia to live healthy lives. The disorder is diagnosed through newborn screening to detect
GLYCOGENOLYSIS & REGULATION OF GLYCOGEN METABOLISM
- 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
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Galactose metabolism disorders
This document discusses galactosemia, a rare genetic disorder that affects the body's ability to process galactose. Galactose is produced when lactose is broken down in the body. Normally it is converted to glucose for energy, but in galactosemia there is a deficiency in the enzyme galactose-1-phosphate uridyltransferase, preventing this process. As a result, galactose builds up in tissues and can cause issues like jaundice, cataracts, intellectual disability and liver/kidney problems. The disorder is treated by removing galactose and lactose from the diet. There are three types of galactosemia based on the specific enzyme deficiency.
Regulation of body glucose
Blood glucose levels are regulated by a balance between the rate of glucose entering and leaving the bloodstream. The pancreas monitors glucose levels and secretes insulin when levels rise, which lowers glucose by promoting uptake and storage, and glucagon when levels fall, which raises glucose. Other hormones like cortisol, epinephrine, growth hormone and thyroid hormones also influence glucose levels. Deviations can lead to hyperglycemia or hypoglycemia and diseases like diabetes.
GLACTOSE METABOLISM
Galactosemia is a condition where the body cannot break down the sugar galactose found in milk. Symptoms include jaundice, vomiting, poor weight gain, irritability, and seizures. The treatment is removing all foods containing galactose from the diet through avoiding milk and milk products. There is no cure, but following a strict lactose-free diet can control the condition.
Metabolic effects of diabetes mellitus
Metabolic changes in diabetes result from insulin deficiency and profoundly affect the liver, muscle, and adipose tissue. This leads to hyperglycemia and ketoacidosis as the liver produces glucose while tissues cannot utilize it. It also causes increased mobilization of fatty acids from adipose tissue and their breakdown in the liver, resulting in the production of ketone bodies. Excess fatty acids are also converted to triglycerides and secreted into the bloodstream. The insulin deficiency shifts energy production away from carbohydrate metabolism and towards fat oxidation, cholesterol synthesis, and ketone body synthesis.
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The document summarizes digestion and absorption of carbohydrates. Carbohydrates are broken down into monosaccharides like glucose in the mouth by saliva and in the small intestine by pancreatic enzymes. Glucose is then absorbed into the bloodstream through active transport using sodium-glucose transporters in the intestine or facilitative transport depending on concentration gradients across the intestinal wall. Different glucose transporters (GLUTs) are responsible for transporting glucose and other sugars into tissues throughout the body.
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GALACTOSE AND FRUCTOSE(2).pptx
- Galactose is obtained through the diet primarily from lactose in milk and is metabolized mainly in the liver. It is converted to glucose through a series of enzymatic reactions involving galactokinase, galactose-1-phosphate uridylyltransferase, and UDP-glucose 4-epimerase.
- Deficiencies of galactokinase or galactose-1-phosphate uridylyltransferase can cause galactosemia, leading to an accumulation of galactose and its metabolites in tissues and symptoms including liver damage, cataracts, and intellectual disability.
- Fructose obtained through the diet is converted to glucose mainly in the liver
FRUCTOSE METABOLISM
Fructose is metabolized primarily in the liver and small intestine. In the liver, fructose is converted to fructose-1-phosphate by fructokinase using ATP as energy. Fructose-1-phosphate is then cleaved by aldolase B into glyceraldehyde and dihydroxyacetone phosphate, which both enter glycolysis to generate energy. This pathway allows fructose to be rapidly metabolized and generates intermediates for glycolysis, though it requires two ATP per fructose molecule. Disorders of this pathway can cause hypoglycemia or liver failure if not treated by avoiding dietary fructose and sucrose.
Glucose Transporters.pptx
Glucose transporters are a wide group of membrane proteins that facilitate the transport of glucose across the plasma membrane, a process known as facilitated diffusion. Because glucose is a vital source of energy for all life, these transporters are present in all phyla.
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1. The pancreas contains clusters of cells called islets of Langerhans that secrete hormones like insulin and glucagon to regulate blood glucose levels. Insulin allows cells to take in glucose from the bloodstream and lowers blood glucose levels, while glucagon has the opposite effect.
2. In diabetes, the pancreas either produces little or no insulin (type 1 diabetes) or the body develops a resistance to insulin's effects (type 2 diabetes), disrupting the body's ability to regulate blood glucose levels and maintain homeostasis. This leads to high blood glucose levels (hyperglycemia).
3. Without enough insulin to allow cells to take in glucose, the body begins to breakdown proteins and fats
Regulation of blood glucose
Blood glucose levels are normally maintained within a narrow range through the regulation of glucose entry into and removal from the bloodstream. Hormones like insulin and glucagon act in opposition to maintain glucose homeostasis, with insulin lowering blood glucose through promoting glucose uptake in cells and glucagon raising it through stimulating glucose production and release from the liver. A variety of tissues, including muscle, adipose, liver, and brain, play roles in glucose regulation through uptake, storage, production, and utilization of glucose.
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This document provides an overview of carbohydrate metabolism and disorders by Dr. Elham Sharif. It covers objectives, carbohydrate classification and functions, glucose metabolism pathways, hormonal control of glucose levels, normal blood glucose and urine glucose levels, hormones that affect blood glucose, abnormalities in carbohydrate metabolism including lactose intolerance and hypoglycemia, causes and symptoms of diabetes mellitus, and classification of diabetes into type 1 and type 2. The key topics covered include glucose regulation by insulin and glucagon, glucose metabolism pathways in the body, and abnormalities related to carbohydrate metabolism and diabetes.
Glucose receptors1
There are 13 glucose transporter proteins (GLUTs) that transport glucose across cell membranes. They are divided into 3 classes. Class I includes GLUT1-4, the most well studied of which are GLUT1, GLUT2, GLUT3 and GLUT4. GLUT1 transports glucose across the blood-brain barrier. GLUT2 acts as a bidirectional transporter in the liver and pancreas. GLUT3 transports glucose into neurons. GLUT4 is the insulin-regulated transporter that transports glucose into muscle and fat cells for storage. Defects in these transporters can lead to diseases like diabetes.
Inborn errors of carbohydrate metabolism
Glycogen storage diseases, Congenital galactosaemia, Galactokinase deficiency, Essential fructosuria, Hereditary fructose intolerance, Essential pentosuria
Galactosemia
Galactosemia is a rare genetic disorder caused by a deficiency of the enzyme galactose-1-phosphate uridylyl transferase (GALT). This enzyme is needed to break down the sugar galactose. Without it, galactose builds up and causes serious health issues. The disorder is inherited in an autosomal recessive pattern and affects how the body processes lactose from milk. Symptoms in infants can include vomiting, jaundice, and failure to thrive if not treated early through a strict lactose-free diet. While not curable, dietary management throughout life can prevent complications and allow those with galactosemia to live healthy lives. The disorder is diagnosed through newborn screening to detect
GLYCOGENOLYSIS & REGULATION OF GLYCOGEN METABOLISM
- 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
Glycogen storage diseases
Glycogen storage diseases are caused by defects in glycogen synthesis or breakdown. There are several types affecting the liver or muscle. Type I is caused by glucose-6-phosphatase deficiency leading to liver enlargement and low blood sugar during fasting. Type III involves a debranching enzyme defect causing swollen abdomen and muscle weakness. Type VI deficiency of liver phosphorylase causes hepatomegaly, hypoglycemia, and growth issues. Symptoms, diagnosis, and treatments vary depending on the specific enzyme deficiency and tissues involved.
Galactose metabolism disorders
This document discusses galactosemia, a rare genetic disorder that affects the body's ability to process galactose. Galactose is produced when lactose is broken down in the body. Normally it is converted to glucose for energy, but in galactosemia there is a deficiency in the enzyme galactose-1-phosphate uridyltransferase, preventing this process. As a result, galactose builds up in tissues and can cause issues like jaundice, cataracts, intellectual disability and liver/kidney problems. The disorder is treated by removing galactose and lactose from the diet. There are three types of galactosemia based on the specific enzyme deficiency.
Regulation of body glucose
Blood glucose levels are regulated by a balance between the rate of glucose entering and leaving the bloodstream. The pancreas monitors glucose levels and secretes insulin when levels rise, which lowers glucose by promoting uptake and storage, and glucagon when levels fall, which raises glucose. Other hormones like cortisol, epinephrine, growth hormone and thyroid hormones also influence glucose levels. Deviations can lead to hyperglycemia or hypoglycemia and diseases like diabetes.
GLACTOSE METABOLISM
Galactosemia is a condition where the body cannot break down the sugar galactose found in milk. Symptoms include jaundice, vomiting, poor weight gain, irritability, and seizures. The treatment is removing all foods containing galactose from the diet through avoiding milk and milk products. There is no cure, but following a strict lactose-free diet can control the condition.
Metabolic effects of diabetes mellitus
Metabolic changes in diabetes result from insulin deficiency and profoundly affect the liver, muscle, and adipose tissue. This leads to hyperglycemia and ketoacidosis as the liver produces glucose while tissues cannot utilize it. It also causes increased mobilization of fatty acids from adipose tissue and their breakdown in the liver, resulting in the production of ketone bodies. Excess fatty acids are also converted to triglycerides and secreted into the bloodstream. The insulin deficiency shifts energy production away from carbohydrate metabolism and towards fat oxidation, cholesterol synthesis, and ketone body synthesis.
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The document provides an overview of carbohydrate metabolism. It discusses the main dietary sources of carbohydrates and their functions, including providing energy. It describes the digestion of carbohydrates by salivary, pancreatic and intestinal enzymes into monosaccharides that are absorbed into the bloodstream. Glucose and galactose enter cells via active transport while fructose uses facilitated diffusion. The liver plays a key role in carbohydrate metabolism, storing glucose and releasing it into circulation. Tissues take up glucose via different glucose transporters. The document outlines several major pathways involved in carbohydrate metabolism.
Digestion & absorption of carbohydrate
This document summarizes the digestion and absorption of carbohydrates. It begins by outlining the types of carbohydrates present in the diet and how they are broken down by enzymes into simpler monosaccharides. It then details the specific enzymes involved in digesting carbohydrates at each step, from salivary amylase in the mouth to pancreatic amylase and disaccharidases in the small intestine. Absorption of monosaccharides like glucose, galactose and fructose occurs via active transport in the intestinal epithelium. Clinical examples like lactose intolerance are also discussed.
Glutes for glucose transporters
Glucose transporters facilitate the transport of glucose across plasma membranes and are present in all life forms. The GLUT family of transporter proteins are found in most mammalian cells and help with basal glucose uptake in tissues like brain and muscle in an insulin-independent manner. Specific GLUT transporters are located in tissues including liver, muscle and fat, and their activity levels are regulated by insulin to control glucose uptake and transport following a meal.
GLUT.pptx
- Glucose transporters (GLUTs) facilitate the movement of glucose across cellular membranes into tissues and organs. The main GLUTs are GLUT1-5 which have tissue-specific expression and functions.
- GLUT1 transports glucose into tissues like red blood cells and brain. GLUT2 transports glucose bidirectionally between blood and liver/kidney/pancreas cells. GLUT3 specifically transports glucose into neurons. GLUT4 is responsible for insulin-dependent glucose uptake into adipose tissue and skeletal muscle. GLUT5 transports fructose in the small intestine and testes.
- Insulin signaling stimulates the translocation of intracellular GLUT4 vesicles to the cell surface membrane, increasing glucose uptake into muscles and fat
DIGESTION & ABSORPTION OF CARBOHYDRATES
Carbohydrates are digested in the mouth by salivary amylase and in the small intestine by pancreatic amylase and intestinal enzymes. Monosaccharides like glucose are absorbed into the bloodstream through active transport involving sodium-glucose transporters in the intestinal walls. Glucose is the primary fuel for cells and its uptake is mediated by glucose transporters, especially GLUT2 and GLUT4 which are regulated by insulin. Deficiencies in disaccharide-digesting enzymes can cause issues like lactose intolerance and related symptoms.
carbohydrate metabolism lecture 1
This document provides an overview of carbohydrate metabolism, specifically the digestion and absorption of carbohydrates. It describes the processes of carbohydrate digestion in the mouth, stomach, and small intestine by salivary amylase, gastric acid, pancreatic amylase, and intestinal disaccharidases. Absorption occurs primarily as monosaccharides via passive diffusion, facilitated diffusion using glucose transporters, and active transport against gradients using sodium-glucose cotransporters. Lactose intolerance results from lactase deficiency in adulthood.
Carbohydrates ii
Carbohydrates (also called carbs) are a type of macronutrient found in certain foods and drinks. Sugars, starches and fiber are carbohydrates. Other macronutrients include fat and protein. Your body needs these macronutrients to stay healthy.
CHO metabolism206-2005.ppt
Carbohydrates provide the largest source of calories and include starch, lactose, and sucrose. The small intestine breaks down carbohydrates into monosaccharides like glucose through digestion by enzymes attached to the intestinal wall. These monosaccharides are then absorbed into the bloodstream and transported to tissues like muscle and liver to be used for energy or stored as glycogen for later use.
Hormones of the git
This document discusses the hormones of the gastrointestinal tract. It begins by introducing the gastrointestinal endocrine system and hormone receptors. It then discusses several families of hormones, including gastrin-cholecystokinin, pancreatic polypeptide, tachykinin, somatostatin, and secretin. For each hormone, it describes where it is produced, what stimulates its secretion, its targets and effects, and potential clinical applications. The document provides a comprehensive overview of the major hormones in the gastrointestinal system and their functions.
002 carbohydrate Metabolism 1.ppt
The document summarizes carbohydrate metabolism. It discusses the digestion, absorption, and utilization of carbohydrates. Carbohydrate digestion occurs via salivary and pancreatic amylases in the mouth and small intestine, breaking down starches and glycogen into disaccharides and trisaccharides that are then further broken down by intestinal enzymes. Absorption occurs mainly in the jejunum via both active and facilitated transport. Glucose is then distributed to tissues via the bloodstream and undergoes glycolysis and other pathways to produce energy or be used for biosynthesis. Glycolysis is discussed in detail, including its regulation by key enzymes and hormones.
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Digestion and Absorption of Carbohydrates- Biochemistry
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The cerebellum contains leaf-like folds called folia. The core of each folium is formed by pink-staining fibers of the white matter. Overlying the white matter are layers that form the cerebellar cortex, including the molecular layer, Purkinje cell layer, and granular cell layer. The cortex is covered by the piamater.
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The thyroid gland is made up of follicles lined by cuboidal epithelium and containing pink staining colloid consisting of thyroglobulin. Between the follicles is connective tissue, and parafollicular cells are present near the follicles.
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Dietary fiber is the indigestible carbohydrate in food that is important for maintaining normal gastrointestinal motility. A diet rich in fiber from vegetables improves bowel regularity, lowers cholesterol by decreasing bile acid reabsorption, and improves glucose tolerance. Fiber may help reduce the risk of colon cancer. The beneficial effects are greater with soluble fiber, and a diet containing at least 30 grams of fiber per day from vegetables and greens is recommended.
Histology of Tooth
The document discusses the anatomy of teeth. It states that teeth are composed of enamel, dentine, and pulp. The majority of the hard tissue in teeth is dentine, a specialized calcified tissue derived from mesenchyme. The dentine in the root is covered by cementum, another calcified tissue derived from mesenchyme. Teeth are connected to bone by the periodontal ligament, which embeds the tooth in the alveolar ridge.
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The document discusses the musculature of the tongue, noting that it consists of both intrinsic and extrinsic muscles. It states that each half of the tongue contains four intrinsic muscles that change the shape of the tongue from within, and four extrinsic muscles that take origin outside the tongue and move and alter its shape. The four intrinsic muscles are named as the superior longitudinal, inferior longitudinal, transverse, and vertical muscles. The four extrinsic muscles are named as the genioglossus, hyoglossus, styloglossus, and palatoglossus.
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The document discusses the laryngeal muscles, which are divided into extrinsic and intrinsic muscles. The extrinsic muscles attach the larynx to surrounding structures and move the larynx as a whole, while the intrinsic muscles attach the laryngeal cartilages to each other and are responsible for their individual movements. The intrinsic muscles can be further divided based on their actions of opening/closing the laryngeal inlet, adducting/abducting the vocal cords, and increasing/decreasing vocal cord tension. Specific intrinsic muscles and their functions are described.
Infratemporal Fossa
The infratemporal fossa is the space beneath the skull between the pharynx wall and mandible ramus. It communicates with the temporal fossa through a gap behind the zygomatic arch. The fossa is also known as the parapharyngeal or lateral pharyngeal space. It has a roof formed by the sphenoid wing pierced by two foramina, medial wall formed by the lateral pterygoid plate, lateral wall by the mandible ramus, and anterior wall by the maxilla separated from the roof by an orbital fissure. The floor is open and extends to the mandible base, and the posterior wall is formed by the temporal bone styloid process.
Soft Palate
The soft palate is a mobile muscular flap that hangs from the posterior hard palate. It separates the nasopharynx from the oropharynx. It consists of mucous membrane enclosing five pairs of muscles. The soft palate has roles in swallowing, breathing, modifying voice quality, and protecting the nasal mucosa during sneezing and coughing. It receives its blood supply from the lesser palatine, facial, and ascending pharyngeal arteries and innervation from the vagus and glossopharyngeal nerves.
Structure of Hemoglobin
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Sickle Cell Disease
This document discusses sickle cell disease, which is caused by a single point mutation that changes the amino acid glutamic acid to valine in the beta chain of hemoglobin. This causes hemoglobin to polymerize within red blood cells and distort them into a sickle shape. Heterozygous carriers have the sickle cell trait and are common in parts of Africa and India, and it provides protection against malaria, while homozygous individuals experience life-threatening complications like occlusion of blood vessels. Diagnosis involves electrophoresis or a sickling test, and management relies on blood transfusions and medications that interfere with hemoglobin polymerization.
Median Nasal Septum
The nasal septum is the median partition that divides the nasal cavity into two sides. It has bony, cartilaginous, and membranous components. The bony parts include the perpendicular plate of the ethmoid and the vomer. The cartilaginous parts include the septal cartilage and the medial crura of the alar cartilages, which join to form the columella. The membranous septum lies inferior to the septal cartilage. The nasal septum receives its blood supply from branches of the ophthalmic and maxillary arteries and its innervation from branches of the anterior ethmoidal, nasociliary, pterygopalatine, and maxillary nerves.
Scalenus Anterior
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Scalenus Medius
The scalenus medius is the longest and largest of the scalene muscles. It originates from the posterior tubercles of the transverse processes of C2-C6 vertebrae and inserts on the upper surface of the first rib between the tubercle and groove for the subclavian artery. It is supplied by the ventral rami of C3-C8 spinal nerves and acts to bend the neck to the side when the first rib is fixed or elevate the first rib as an accessory muscle of respiration when its upper end is fixed.
Scalenus Posterior
The scalenus posterior muscle originates from the posterior tubercles of the transverse processes of C4 to C6 vertebrae. It inserts on the outer surface of the second rib behind the tubercle for serratus anterior. The scalenus posterior is innervated by the ventral rami of C6 to C8 spinal nerves. It functions to bend the cervical vertebral column to the side when the second rib is fixed, and helps elevate the second rib to act as an accessory muscle of respiration when its upper attachment is fixed.
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Glucose Transporters
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- 3. Transporter Present in Properties GluT1 RBC, Brain, Kidney, Colon, Retina, Placenta Glucose Uptake In Most Of Cells GluT2 Serosal Surface Of Intestinal Cells, Liver Beta Cells Of Pancreas •Low Affinity •Glucose Uptake In Liver •Glucose Sensor In Beta Cells GluT3 Neurons, Brain •High Affinity •Glucose Into Brain Cells GluT4 Skeletal, Heart Muscle, Adipose Tissue Insulin Mediated Glucose Uptake GluT5 Small Intestine, Testis, Sperms, Kidney •Fructose Transporter •Poor Ability To Transport Glucose GluT7 Liver Endoplasmic Reticulum Glucose From ER To Cytoplasm SGluT Intestine, Kidney Cotransport - From Lumen Into Cell Rashmi Priyem Saravanan
- 5. SGluT-1 Absorption from intestinal lumen into intestinal cell is by co-transport mechanism (secondary active transport). A membrane bound carrier protein is involved, which carries glucose, along with sodium. This sodium is later expelled by the sodium pump with utilization of energy. So energy is needed indirectly . The Transporter in Intestine is named as SGluT- 1. Involved in Glucose-Galactose Malabsorption. Rashmi Priyem Saravanan
- 6. SGluT-1 Absorption from intestinal lumen into intestinal cell is by co-transport mechanism (secondary active transport). A membrane bound carrier protein is involved, which carries glucose, along with sodium. This sodium is later expelled by the sodium pump with utilization of energy. So energy is needed indirectly . The Transporter in the Kidney is called SGluT-2. The SGluT-2 is defective in Congenital Renal Glycosuria. Rashmi Priyem Saravanan