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BLOOD SUGAR HOMEOSTASIS

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BLOOD SUGAR HOMEOSTASIS


  NORMAL BLOOD GLUCOSE CONCENTRATIONS
•Fasting plasma glucose (post absorptive glucose, 12 hrs after overnight meal) is in the range of 70-110 mg/dl.

•Postprandial plasma glucose (2 hrs after meal) is less than 140 mg/dl.

•Hypoglycemia refers to plasma glucose levels below fasting level but symptoms are usually seen when the levels fall below50mg/dl. 
•Renal threshold for glucose is 180 mg/dl.

SIGNIFICANCE OF BLOOD GLUCOSE HOMEOSTASIS

•Energy provision to glucose  dependent tissues.

• Maintenance of the plasma glucose concentrations within narrow limits is essential for health.

•Hypoglycemia is dangerous because glucose is the primary energy substrates of the brain and erythrocytes.

•The brain is vulnerable to hypoglycemia because it cannot utilize circulating fatty acids as an energy sources.

•Although ketone bodies are oxidized by the brain, development of ketosis requires number of hours so that the pathway is not effective against acute hypoglycemia.

PATHWAYS OF BLOOD GLUCOSE HOMEOSTASIS

•Blood glucose homeostasis is dependent on the balance between the pathways that cause entry of glucose into the blood and the pathways that cause removal of glucose from blood.

SOURCES OF BLOOD GLUCOSE

•Pathways that cause entry of glucose to blood are:

1.Digestion/absorption of dietary carbohydrates

2.Breakdown of glycogen to glucose in the liver (glycogenolysis:hepatic)

3.Synthesis of glucose from non-carbohydrates (gluconeogenesis)

4.Metabolism of galactose  and fructose to glucose in the liver.

UTILIZATION OF BLOOD GLUCOSE

•Pathways for the removal of glucose from blood are:

1.Peripheral uptake of glucose (in muscle, adipose tissue, etc.)

2.Oxidation of glucose

3.Synthesis of glycogen (glycogenesis)

4.Conversion of glucose to fat (lipogenesis) 

fig:overview of regulation of blood glucose


 
 











 fig:Homeostasis of blood glucose


HORMONAL CONTROL OF BLOOD GLUCOSE HOMEOSTASIS
•Hormones that regulate blood glucose are of two types:
1.  Hypoglycemic hormones
•Hypoglycemic hormone is:
i. Insulin.
2.  Hyperglycemic hormones
•Hyperglycemic hormones are
i.Glucagon
ii. Epinephrine
iii. Cortisol
iv. ACTH,
v.Growth hormone and
vi.Thyroxine.
 

1.INSULIN
Chemistry
•Insulin is a polypeptide hormone.
Source
•Insulin is produced by β-cells of Islet of Langerhans.
Stimulus for release
•Insulin is released in response to hyperglycemia.
Mechanisms of Insulin Induced Hypoglycemia
1.Increased peripheral uptake of glucose. Glucose uptake by liver or brain is not dependent on insulin.
2.Increased glycogenesis
3.Suppression of gluconeogenesis
4.Stimulation of lipogenesis
5.   Decreased glycogenolysis
2. GLUCAGON
Chemistry
•Glucagon is a polypeptide hormone.
Source
•Glucagon is produced by α-cells of Islet of Langerhans.
Stimulus for release
•Glucagon is released in response to hypoglycemia.
Mechanism of hyperglycemic effect
•Glucagon increases blood glucose (hyperglycemia) by the following mechanisms:
1.Stimulation of glycogenolysis
2.Stimulation of gluconeogenesis.
3.   Suppression of glycogenesis

3. GLUCOCORTICOIDS (CORTISOL)
Chemistry
•Cortisol is a steroid hormone.
Source
•Cortisol is produced from the adrenal cortex.
Stimulus for release
•Cortisol is released in response to hypoglycemia or stress.
Mechanism of action
•Cortisol increases blood glucose (hyperglycemia) by the following mechanisms:
1.Induction of key gluconeogenic enzymes.
2.Increased transaminase activity (conversion of alanine to pyruvate).
3.Increased availability of alanine by stimulation of muscle proteolysis.
4.Decreased peripheral uptake of glucose.
4. EPINEPHRINE
CHEMISTRY
•Epinephrine is a amine hormone (biogenic amine).
SOURCE
•Epinephrine is produced from adrenal medulla.
STIMULUS FOR RELEASE
•Epinephrine is released in response to stress.
Mechanism of hyperglycemic effect
•Epinephrine increases blood glucose (hyperglycemia) by the following mechanisms:
1. Stimulation of hepatic glycogenolysis.
2. Stimulation of gluconeogenesis..
3. Suppression of sensitivity to the effects of insulin (insulin resistance)
 
 
5. ACTH
Chemistry
•ACTH is a polypeptide.
Source
•ACTH is produced from anterior pituitary.
Stimulus for release
•ACTH is released in response to hypoglycemia and stress.
Mechanism of hyperglycemic effect
•ACTH increases blood glucose (hyperglycemia) by the following mechanisms:
1.  Inhibition of peripheral uptake of glucose
2.  Cortisol induced effects
6. GROWTH HORMONE
Chemistry
•Growth hormone is a polypeptide.
Source
•Growth hormone is produced by the anterior pituitary.
Stimulus for release
•Growth hormone is released in response to hypoglycemia.
Hyperglycemic effect
•Growth hormone increases blood glucose (hyperglycemia) by inhibition of peripheral uptake of glucose.
7. THYROXINE
CHEMISTRY
•Thyroxine is a tyrosine (amino acid) derivative.
SOURCE
•Thyroxine is produced from thyroid gland.
STIMULUS FOR RELEASE
•Thyroxine is released in response to hypoglycemia or stress.
MECHANISM OF HYPERGLYCEMIC EFFECT
•Thyroxine increases blood glucose level (hyperglycemia) by
1.Stimulation of glycogenolysis.
2.Decreased sensitivity to the effects of insulin.
 


 
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