Wednesday, July 30, 2014
Sadifit - a hope for a healthy life?
Sadifit is an Ucranian product what contains natural vegetal products
Composition, structure and packing
collection filter bag 3 g, № 20
collection pack 75 g, int. package
Blueberry shoots 0.2 g / g
Common bean fruit pods 0.2 g / g
Green tea leaf 0.15 g / g
Peppermint leaves 0.05 g / g
Jerusalem artichoke (topinambour) tubers 0.2 g / g
Stevia leaves 0.2 g / g
№ UA/6114/01/01 from 19.03.2007 to 19.03.2012
In addition, regulates the function of the gastrointestinal tract, stimulates the activity of the pancreas, normalizes metabolism, reduces cholesterol levels in the blood, has anti-inflammatory, choleretic and diuretic effects.
To get the needed volume bring boiled water up to 300 ml. Adults take in warm form 1/2 cup 3 times a day 30 minutes before meals for 20-30 days. Children, depending on the age of 2 tablespoons up to 1/3 cup 3 times a day 30 minutes before meals for 20-30 days. Before use, shake the infusion is recommended.
2 packet filter placed in a glass or enamel bowl, pour 300 ml (1.5 cups) of boiling water, cover and insist at least 1 hour Insisting recommended in a thermos. Adults take infusion in warm form 1/2 cup 3 times a day 30 minutes before meals for 20-30 days. Children, depending on age from 2 tablespoons to 1/3 cup 3 times a day 30 minutes before meals for 20-30 days.
After a 7-10 days pause it is recommended to repeat the treatment.
Overdosage
reports of overdose have not been reported.
Drug Interactions
unknown.
Adverse effects
not identified.
Conditions and terms
Store in a dry, dark place. The prepared infusion - in a cool place (8-15 ° C) no more than 2 days.
Shelf life - 2 years.
Statement
light and medium forms of type II diabetes; gastrointestinal diseases (enterocolitis, chronic pancreatitis, chronic cholecystitis).
Contraindications
pregnancy; individual sensitivity to biologically active substances contained in the drug.
Cautions
take in warm form 30 minutes before eating.
Composition, structure and packing
collection pack 75 g, int. package
Blueberry shoots 0.2 g / g
Common bean fruit pods 0.2 g / g
Green tea leaf 0.15 g / g
Peppermint leaves 0.05 g / g
Jerusalem artichoke (topinambour) tubers 0.2 g / g
Stevia leaves 0.2 g / g
№ UA/6114/01/01 from 19.03.2007 to 19.03.2012
Pharmacological action
Collection components contain inulin, amino acids, glycosides, tannins, vitamins, essential oils, flavonoids, saponins, organic acids, micro and macroelements. This complex of biologically active substances has hypoglycemic effect in type II diabetes mellitus with mild and moderate form, allowing in some cases, to reduce the daily dose of oral antidiabetic agents.In addition, regulates the function of the gastrointestinal tract, stimulates the activity of the pancreas, normalizes metabolism, reduces cholesterol levels in the blood, has anti-inflammatory, choleretic and diuretic effects.
The dosage
6 g (1 tablespoon) of collection is placed in an enamel bowl, pour 300 ml (1.5 cups) of hot boiled water, cover with a lid and boil on water bath for 15 min. Cool it at room temperature for 45 minutes, filter, and squeeze the residue to the strained infusion.To get the needed volume bring boiled water up to 300 ml. Adults take in warm form 1/2 cup 3 times a day 30 minutes before meals for 20-30 days. Children, depending on the age of 2 tablespoons up to 1/3 cup 3 times a day 30 minutes before meals for 20-30 days. Before use, shake the infusion is recommended.
2 packet filter placed in a glass or enamel bowl, pour 300 ml (1.5 cups) of boiling water, cover and insist at least 1 hour Insisting recommended in a thermos. Adults take infusion in warm form 1/2 cup 3 times a day 30 minutes before meals for 20-30 days. Children, depending on age from 2 tablespoons to 1/3 cup 3 times a day 30 minutes before meals for 20-30 days.
After a 7-10 days pause it is recommended to repeat the treatment.
Overdosage
reports of overdose have not been reported.
Drug Interactions
unknown.
Adverse effects
not identified.
Conditions and terms
Store in a dry, dark place. The prepared infusion - in a cool place (8-15 ° C) no more than 2 days.
Shelf life - 2 years.
Statement
light and medium forms of type II diabetes; gastrointestinal diseases (enterocolitis, chronic pancreatitis, chronic cholecystitis).
Contraindications
pregnancy; individual sensitivity to biologically active substances contained in the drug.
Cautions
take in warm form 30 minutes before eating.
Monday, July 28, 2014
Effect of Insulin on Fat Metabolism
Effect of Insulin on Fat Metabolism
Although not quite as visible as the acute effects of insulin on carbohydratemetabolism, insulin’s effects on fat metabolism are, in the long run, equally important. Especially dramatic is the long-term effect of insulin lack in causing extreme atherosclerosis, often leading to heart attacks, cerebral strokes, and other vascular accidents. But first, let us discuss the acute effects of insulin on fat metabolism.Insulin Promotes Fat Synthesis and Storage
Insulin has several effects that lead to fat storage in adipose tissue. First, insulin increases the utilization of glucose by most of the body’s tissues, which automatically decreases the utilization of fat, thus functioning as a fat sparer.However, insulin also promotes fatty acid synthesis. This is especially true when more carbohydrates are ingested than can be used for immediate energy, thus providing the substrate for fat synthesis.Almost all this synthesis occurs in the liver cells, and the fatty acids are then transported from the liver by way of the blood lipoproteins to the adipose cells to be stored.
The different factors that lead to increased fatty acid synthesis in the liver include the following:
- Insulin increases the transport of glucose into the liver cells.After the liver glycogen concentration reaches 5 to 6 per cent, this in itself inhibits further glycogen synthesis. Then all the additional glucose entering the liver cells becomes available to form fat. The glucose is first split to pyruvate in the glycolytic pathway, and the pyruvate subsequently is converted to acetyl coenzyme A (acetyl-CoA), the substrate from which fatty acids are synthesized.
- An excess of citrate and isocitrate ions is formed by the citric acid cycle when excess amounts of glucose are being used for energy. These ions then have a direct effect in activating acetyl-CoA carboxylase, the enzyme required to carboxylate acetyl-CoA to form malonyl-CoA, the first stage of fatty acid synthesis.
- Most of the fatty acids are then synthesized within the liver itself and used to form triglycerides,the usual form of storage fat. They are released from the liver cells to the blood in the lipoproteins.
Insulin activates lipoprotein lipase in the capillary walls of the adipose tissue, which splits the triglycerides again into fatty acids, a requirement for them to be absorbed into the adipose cells, where they are again converted to triglycerides and stored.
Role of Insulin in Storage of Fat in the Adipose Cells.
Insulin has two other essential effects that are required for fat storage in adipose cells:1. Insulin inhibits the action of hormone-sensitive lipase. This is the enzyme that causes hydrolysis of
the triglycerides already stored in the fat cells.
Therefore, the release of fatty acids from the adipose tissue into the circulating blood is inhibited.
2. Insulin promotes glucose transport through the cell membrane into the fat cells in exactly the same
ways that it promotes glucose transport into muscle cells.
Some of this glucose is then used to
synthesize minute amounts of fatty acids, but more important, it also forms large quantities of a-glycerol phosphate.
This substance supplies the glycerol that combines with fatty acids to form
the triglycerides that are the storage form of fat in adipose cells.
Therefore, when insulin is not available, even storage of the large amounts of fatty acids transported from the liver in the lipoproteins is almost blocked.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
References:
© Copyright Guyton and Hall Textbook of Medical Physiology - See more at: http://how-to-get-rid-of-diabetes.blogspot.com/2014/07/insulin-promotes-glucose-metabolism.html#sthash.tKI5KMwU.dpuf
© Copyright Guyton and Hall Textbook of Medical Physiology - See more at: http://how-to-get-rid-of-diabetes.blogspot.com/2014/07/insulin-promotes-glucose-metabolism.html#sthash.tKI5KMwU.dpuf
Physiopathology of endocrine pancreas. Insulin resistance
Insulin resistance
Type II diabetes is characterized by dysfunction of pancreatic beta cells and insulin resistance, in the majority of the tissues - peripheral target: skeletal muscle, liver, kidney, adipose tissue.
In insulin resistance ( in people with type II diabetes) the dose of exogenous insulin increases significantly , which stimulate glucose uptake by tissues and inhibits endogenous glucose production.
Insulin resistance reflects the predominant defect in insulin action on skeletal muscles and liver.
The major causes of muscle insulin resistance in prediabetic stage are: genetic predisposition, obesity and physical hypoactivity.
Obesity and lack of exercise are major factors that contribute to the development of insulin resistance. It was established that exercise increases insulin sensitivity independent of body mass reduction and changes in body composition.
Thus, the children of parents with type II diabetes, physical training for 6 weeks increases glucose uptake and glycogen synthesis due to increased sensitivity to insulin.
In case of endocrine gland hyperfunction it is necessary to administer preparations that inhibit gland function (eg Thyrostatic or radioactive iodine treatment - in hyperthyreosis).
Radical treatment involves surgical removal of hormonproductive tumors.
Type II diabetes is characterized by dysfunction of pancreatic beta cells and insulin resistance, in the majority of the tissues - peripheral target: skeletal muscle, liver, kidney, adipose tissue.
In insulin resistance ( in people with type II diabetes) the dose of exogenous insulin increases significantly , which stimulate glucose uptake by tissues and inhibits endogenous glucose production.
Insulin resistance reflects the predominant defect in insulin action on skeletal muscles and liver.
The major causes of muscle insulin resistance in prediabetic stage are: genetic predisposition, obesity and physical hypoactivity.
Obesity and lack of exercise are major factors that contribute to the development of insulin resistance. It was established that exercise increases insulin sensitivity independent of body mass reduction and changes in body composition.
Thus, the children of parents with type II diabetes, physical training for 6 weeks increases glucose uptake and glycogen synthesis due to increased sensitivity to insulin.
Pharmacotherapy Principles of endocrine disorders
The basic principles of pharmacocorection is to restore hormonal homeostasis in the body through substitution treatment in endocrine hypofunction (thyroid hormone in hypothyroidism, estrogen or androgen administration in the hypogonadism, insulin in type I diabetes, etc.).In case of endocrine gland hyperfunction it is necessary to administer preparations that inhibit gland function (eg Thyrostatic or radioactive iodine treatment - in hyperthyreosis).
Radical treatment involves surgical removal of hormonproductive tumors.
Physiopathology of endocrine pancreas. Insulin deficiency
Insulin deficiency
Insulin deficiency is the main cause of insulin-dependent diabetes pathogeny or type I diabetes.
Type I diabetes Mellitus is related to insulin deficiency consecutive to reduction of beta-pancreatic cells population. One of the major causes of diabetes Mellitus is inflammation with autoimmune alteration of Lagerhans islets (insulite). It has a specific and exclusive localisation in islets formed of beta cells, while in islets formed of glucagon producing cells inflammation is missing.
Insulin deficiency produces multiple metabolic disturbances with specific severe lesions of body structure.
Glycogen and lipid synthesis disturbances constitutes the basic and essential metabolic manifestation of insulin deficiency.
These are related with insulin/glucagon index.
The consequence of this thing is the impossibility of liver and muscles to synthesise glycogen and of adipocites to synthesise lipids from glucose.
Cardinal clinical signs of type I diabetes: reduced glucose tolerance, hyperglycaemia, protein catabolism intensification, hyperlipidemia, angiopathy and nephrotic syndrome.
The pathogenesis of hyperglycaemia is the fact that in the absence of insulin, insulin-dependent glucose receptors in adipocytes and myocytes type IV reside in the cytoplasm, are not exposed on the cell membrane, due to which the glucose can not be assimilated by the cells for synthesis of glycogen and fat.
The pathogenesis of hyperlipidemia (prevalent on account of the very low density lipoprotein and non-esterified fatty acids) can be explained by the fact that the lipase in the absence of adipocyte insulin remain phosphorylated, inactive, dietary fat are not incorporated into adipocytes, and unwanted fatty acids are converted in the liver to very low density lipoprotein.Increase blood concentration of non-esterified fatty acids (hyperlipidemia transport) is the consequence of intense mobilization of lipids from adipose tissue.
Hiperketonemia and ketonuria is due to high concentration of fatty acids in the blood with increased beta-oxidation and acetyl CoA abundant production, that in lack of insulin is not used for lipid resynthesis but ketone bodies - acetone, hydroxybutyric acid and acetylacetic acid synthesis.
Renal syndrome in hypoinsulinism is constituted of glucosuria due to hyperglycaemia and high glucose concentration in glomerular filtration, which exceeds the functional capacity of the canalicular epithelium glucokinase (threshold is about 180 mg / dL).
Glucosuria leads polyuria (osmotic diuresis) and polydipsia. Development of diabetic nephropathy with microangiopathy leads to progressive decrease in glomerular filtration rate, with the growth of the permeability of renal filter and albuminuria.
Ketonuria is consecutive to hyperketonemia.
In the pathogenesis of diabetic angiopathy glycosylation of proteins - its IDDM process, which consists in the non-fermentative combination of glucose with amino acids amino-groups to form complexes of glucose and protein (ketone-amino-proteins) in the vessel wall .
Glycosylation changes the conformation of the protein molecule, the electric charge, alter the function of proteins, blocking the active center. Diabetic angiopathy is affecting both small vessels and large ones.
Diabetes can lead to coma - ketoacidotic in absolute insufficiency of insulin, hyperosmolar in moderate insulin deficiency and lactoacidotic in hypoxia, sepsis, cardiogenic shock. (An overdose of insulin can result in hypoglycemic coma).
Pathogenetic correction of homeostasis in ketoacidotic coma seeks liquidation of insulin deficiency, and rehydration and resalinization of the body, restoring acid-base balance and glycogen reserves.
Sunday, July 20, 2014
Lack of Effect of Insulin on Glucose Uptake and Usage by the Brain
Lack of Effect of Insulin on Glucose Uptake
and Usage by the Brain
The brain is quite different from most other tissues of the body in that insulin has little effect on uptake or
use of glucose. Instead, the brain cells are permeable to glucose and can use glucose without the intermediation of insulin.
The brain cells are also quite different from most other cells of the body in that they normally use only
glucose for energy and can use other energy substrates, such as fats, only with difficulty.
Therefore, it is essential that the blood glucose level always be maintained above a critical level, which is one of the most important functions of the blood glucose control system.
When the blood glucose falls too low, into
the range of 20 to 50 mg/100 ml, symptoms of hypoglycemic shock develop, characterized by progressive
nervous irritability that leads to fainting, seizures, and even coma.
Effect of Insulin on Carbohydrate Metabolism
in Other Cells
Insulin increases glucose transport into and glucose usage by most other cells of the body (with the exception of the brain cells, as noted) in the same way that it affects glucose transport and usage in muscle cells.
The transport of glucose into adipose cells mainly provides substrate for the glycerol portion of the fat molecule.
Therefore, in this indirect way, insulin promotes deposition of fat in these cells.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
and Usage by the Brain
The brain is quite different from most other tissues of the body in that insulin has little effect on uptake or
use of glucose. Instead, the brain cells are permeable to glucose and can use glucose without the intermediation of insulin.
The brain cells are also quite different from most other cells of the body in that they normally use only
glucose for energy and can use other energy substrates, such as fats, only with difficulty.
Therefore, it is essential that the blood glucose level always be maintained above a critical level, which is one of the most important functions of the blood glucose control system.
When the blood glucose falls too low, into
the range of 20 to 50 mg/100 ml, symptoms of hypoglycemic shock develop, characterized by progressive
nervous irritability that leads to fainting, seizures, and even coma.
Effect of Insulin on Carbohydrate Metabolism
in Other Cells
Insulin increases glucose transport into and glucose usage by most other cells of the body (with the exception of the brain cells, as noted) in the same way that it affects glucose transport and usage in muscle cells.
The transport of glucose into adipose cells mainly provides substrate for the glycerol portion of the fat molecule.
Therefore, in this indirect way, insulin promotes deposition of fat in these cells.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
Insulin promotes Glucose metabolism
Insulin Promotes Liver Uptake, Storage, and
Use of Glucose
One of the most important of all the effects of insulin is to cause most of the glucose absorbed after a meal
to be stored almost immediately in the liver in the form of glycogen. Then, between meals, when food is
not available and the blood glucose concentration begins to fall, insulin secretion decreases rapidly and
the liver glycogen is split back into glucose, which is released back into the blood to keep the glucose concentration from falling too low.
The mechanism by which insulin causes glucose uptake and storage in the liver includes several almost
simultaneous steps:
1. Insulin inactivates liver phosphorylase,the principal enzyme that causes liver glycogen to
split into glucose. This prevents breakdown of the glycogen that has been stored in the liver cells.
2. Insulin causes enhanced uptake of glucose from the blood by the liver cells. It does this by
increasing the activity of the enzyme glucokinase, which is one of the enzymes that causes the initial
phosphorylation of glucose after it diffuses into the liver cells. Once phosphorylated, the glucose is
temporarily trapped inside the liver cells because phosphorylated glucose cannot diffuse back
through the cell membrane.
3. Insulin also increases the activities of the enzymes that promote glycogen synthesis, including
especially glycogen synthase, which is responsible for polymerization of the monosaccharide units to
form the glycogen molecules.
The net effect of all these actions is to increase the amount of glycogen in the liver. The glycogen can
increase to a total of about 5 to 6 per cent of the liver mass,which is equivalent to almost 100 grams of stored glycogen in the whole liver.
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Glucose Is Released from the Liver Between Meals.
When the blood glucose level begins to fall to a low level between meals, several events transpire that cause the liver to release glucose back into the circulating blood:
1. The decreasing blood glucose causes the pancreas to decrease its insulin secretion.
2. The lack of insulin then reverses all the effects listed earlier for glycogen storage, essentially stopping further synthesis of glycogen in the liver and preventing further uptake of glucose by the liver from the blood.
3. The lack of insulin (along with increase of glucagon, which is discussed later) activates the enzyme phosphorylase, which causes the splitting of glycogen into glucose phosphate.
4. The enzyme glucose phosphatase, which had been inhibited by insulin, now becomes activated by the
insulin lack and causes the phosphate radical to split away from the glucose; this allows the free glucose to diffuse back into the blood.
Thus, the liver removes glucose from the blood when it is present in excess after a meal and returns it to the blood when the blood glucose concentration falls between meals. Ordinarily, about 60 per cent of
the glucose in the meal is stored in this way in the liver and then returned later.
Insulin Promotes Conversion of Excess Glucose into Fatty Acids and Inhibits Gluconeogenesis in the Liver.
When the quantity of glucose entering the liver cells is more than can be stored as glycogen or can be used for local hepatocyte metabolism, insulin promotes the conversion of all this excess glucose into fatty acids.
These fatty acids are subsequently packaged as triglycerides in very-low-density lipoproteins and transported in this form by way of the blood to the adipose tissue and deposited as fat.
Insulin also inhibits gluconeogenesis. It does this mainly by decreasing the quantities and activities of the liver enzymes required for gluconeogenesis.
However, part of the effect is caused by an action of insulin that decreases the release of amino acids
from muscle and other extrahepatic tissues and in turn the availability of these necessary precursors
required for gluconeogenesis. This is discussed further in relation to the effect of insulin on protein
metabolism.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
Use of Glucose
One of the most important of all the effects of insulin is to cause most of the glucose absorbed after a meal
to be stored almost immediately in the liver in the form of glycogen. Then, between meals, when food is
not available and the blood glucose concentration begins to fall, insulin secretion decreases rapidly and
the liver glycogen is split back into glucose, which is released back into the blood to keep the glucose concentration from falling too low.
The mechanism by which insulin causes glucose uptake and storage in the liver includes several almost
simultaneous steps:
1. Insulin inactivates liver phosphorylase,the principal enzyme that causes liver glycogen to
split into glucose. This prevents breakdown of the glycogen that has been stored in the liver cells.
2. Insulin causes enhanced uptake of glucose from the blood by the liver cells. It does this by
increasing the activity of the enzyme glucokinase, which is one of the enzymes that causes the initial
phosphorylation of glucose after it diffuses into the liver cells. Once phosphorylated, the glucose is
temporarily trapped inside the liver cells because phosphorylated glucose cannot diffuse back
through the cell membrane.
3. Insulin also increases the activities of the enzymes that promote glycogen synthesis, including
especially glycogen synthase, which is responsible for polymerization of the monosaccharide units to
form the glycogen molecules.
The net effect of all these actions is to increase the amount of glycogen in the liver. The glycogen can
increase to a total of about 5 to 6 per cent of the liver mass,which is equivalent to almost 100 grams of stored glycogen in the whole liver.
When the blood glucose level begins to fall to a low level between meals, several events transpire that cause the liver to release glucose back into the circulating blood:
1. The decreasing blood glucose causes the pancreas to decrease its insulin secretion.
2. The lack of insulin then reverses all the effects listed earlier for glycogen storage, essentially stopping further synthesis of glycogen in the liver and preventing further uptake of glucose by the liver from the blood.
3. The lack of insulin (along with increase of glucagon, which is discussed later) activates the enzyme phosphorylase, which causes the splitting of glycogen into glucose phosphate.
4. The enzyme glucose phosphatase, which had been inhibited by insulin, now becomes activated by the
insulin lack and causes the phosphate radical to split away from the glucose; this allows the free glucose to diffuse back into the blood.
Thus, the liver removes glucose from the blood when it is present in excess after a meal and returns it to the blood when the blood glucose concentration falls between meals. Ordinarily, about 60 per cent of
the glucose in the meal is stored in this way in the liver and then returned later.
Insulin Promotes Conversion of Excess Glucose into Fatty Acids and Inhibits Gluconeogenesis in the Liver.
When the quantity of glucose entering the liver cells is more than can be stored as glycogen or can be used for local hepatocyte metabolism, insulin promotes the conversion of all this excess glucose into fatty acids.
These fatty acids are subsequently packaged as triglycerides in very-low-density lipoproteins and transported in this form by way of the blood to the adipose tissue and deposited as fat.
Insulin also inhibits gluconeogenesis. It does this mainly by decreasing the quantities and activities of the liver enzymes required for gluconeogenesis.
However, part of the effect is caused by an action of insulin that decreases the release of amino acids
from muscle and other extrahepatic tissues and in turn the availability of these necessary precursors
required for gluconeogenesis. This is discussed further in relation to the effect of insulin on protein
metabolism.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
Saturday, July 19, 2014
Effect of Insulin on Carbohydrate Metabolism
Immediately after a high-carbohydrate meal, the glucose that is absorbed into the blood causes rapid
secretion of insulin, which is discussed in detail later in the chapter.The insulin in turn causes rapid uptake,
storage, and use of glucose by almost all tissues of the body, but especially by themuscles, adipose tissue, and liver.
Insulin Promotes Muscle Glucose Uptake
and Metabolism
During much of the day, muscle tissue depends not on glucose for its energy but on fatty acids. The principal
reason for this is that the normal resting muscle membrane is only slightly permeable to glucose, except
when the muscle fiber is stimulated by insulin; between meals, the amount of insulin that is secreted is too
small to promote significant amounts of glucose entry into the muscle cells.
However, under two conditions the muscles do use large amounts of glucose. One of these is during moderate or heavy exercise.This usage of glucose does not require large amounts of insulin, because exercising muscle fibers become more permeable to glucose even in the absence of insulin because of the contraction process itself.
The second condition for muscle usage of large amounts of glucose is during the few hours after a
meal. At this time the blood glucose concentration is high and the pancreas is secreting large quantities of
insulin. The extra insulin causes rapid transport of glucose into the muscle cells. This causes the muscle
cell during this period to use glucose preferentially over fatty acids, as we discuss later.
Storage of Glycogen in Muscle.
If the muscles are not exercising after a meal and yet glucose is transported into the muscle cells in abundance, then most of the glucose is stored in the form of muscleglycogen instead of being used for energy, up to a limit of 2 to 3 per cent concentration. The glycogen can later be used for energy by the muscle. It is especially useful for short periods of extreme energy use by the muscles and even to provide spurts of anaerobic energy for a few minutes at a time by glycolytic breakdown of the glycogen to lactic acid, which can occur even in the absence of oxygen.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
secretion of insulin, which is discussed in detail later in the chapter.The insulin in turn causes rapid uptake,
storage, and use of glucose by almost all tissues of the body, but especially by themuscles, adipose tissue, and liver.
Insulin Promotes Muscle Glucose Uptake
and Metabolism
During much of the day, muscle tissue depends not on glucose for its energy but on fatty acids. The principal
reason for this is that the normal resting muscle membrane is only slightly permeable to glucose, except
when the muscle fiber is stimulated by insulin; between meals, the amount of insulin that is secreted is too
small to promote significant amounts of glucose entry into the muscle cells.
However, under two conditions the muscles do use large amounts of glucose. One of these is during moderate or heavy exercise.This usage of glucose does not require large amounts of insulin, because exercising muscle fibers become more permeable to glucose even in the absence of insulin because of the contraction process itself.
The second condition for muscle usage of large amounts of glucose is during the few hours after a
meal. At this time the blood glucose concentration is high and the pancreas is secreting large quantities of
insulin. The extra insulin causes rapid transport of glucose into the muscle cells. This causes the muscle
cell during this period to use glucose preferentially over fatty acids, as we discuss later.
Storage of Glycogen in Muscle.
If the muscles are not exercising after a meal and yet glucose is transported into the muscle cells in abundance, then most of the glucose is stored in the form of muscleglycogen instead of being used for energy, up to a limit of 2 to 3 per cent concentration. The glycogen can later be used for energy by the muscle. It is especially useful for short periods of extreme energy use by the muscles and even to provide spurts of anaerobic energy for a few minutes at a time by glycolytic breakdown of the glycogen to lactic acid, which can occur even in the absence of oxygen.
References:
© Copyright Guyton and Hall Textbook of Medical Physiology
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