Blood Glucose Homeostasis

Study Notes

Blood Glucose Homeostasis

Normal blood glucose levels range from 75-110 mg/dl.
After a carbohydrate meal, blood glucose levels can reach 120-135 mg/dl.
Blood glucose originates from the diet (carbohydrates), glycogenolysis in the liver and kidneys, and gluconeogenesis in the liver and kidneys.
The gastrointestinal tract plays a role in glucose homeostasis by delaying the evacuation of food after a meal, preventing sudden hyperglycemia.
Glucose absorption from the intestines is approximately 1 g/kg body weight per hour.
Incretins, GLP-1 and GIP, are involved in glucose homeostasis.
The liver is freely permeable to glucose through GLUT-2 transporters.
Skeletal muscle converts glucose into glycogen and triglycerides. During fasting, glucose is converted to lactic acid and alanine in the muscle.
Adipose tissue utilizes lipolysis to convert triglycerides into glycerol, which can be converted to glucose. During fasting, glucose uptake is increased, and glucose is converted to dihydroxyacetone phosphate and then to triglycerides.
The kidneys participate in gluconeogenesis and reabsorb glucose from the proximal renal tubules via SGLT-1 transporters as long as blood glucose levels remain below 160 mg/dl, known as the renal threshold.
Insulin is secreted during fasting and stress to elevate blood glucose levels. Its actions include inhibiting gluconeogenesis, glycogenolysis, stimulating glycogen synthesis, and inhibiting glucagon.
Glucagon is stimulated by low glucose levels and epinephrine. It inhibits glycolysis and glycogen synthesis while stimulating gluconeogenesis.
Glucagon acts by binding to cell membrane receptors on hepatocytes, increasing cAMP levels.
Epinephrine blocks insulin secretion by beta cells and stimulates glycogenolysis in the liver and muscles.
Corticosteroids and growth hormone stimulate gluconeogenesis.
Thyroxine decreases glucose uptake, leading to hyperglycemia.
Diabetes mellitus, a metabolic disturbance characterized by fasting glucose levels above 126 mg/dl, results from insufficient insulin release or insulin resistance.
Type 1 Diabetes and Type 2 Diabetes are distinct types of diabetes mellitus.

Biochemical Disturbances of Diabetes Mellitus

Insulin deficiency leads to decreased glucose uptake by tissues, reduced glucose oxidation, and increased gluconeogenesis and glycogenolysis.
Increased intracellular glucose results in hyperglycemia and polyphagia (excessive eating).
Insulin deficiency also leads to increased protein breakdown, causing muscle wasting and excessive tissue protein breakdown.
Reduced fatty acid synthesis and increased lipolysis in adipose tissue occur due to insulin deficiency, mobilizing fatty acids and glycerol into the blood, which are transported to the liver and other tissues.
Delayed wound healing, hypolipidemia, and weight loss are further consequences of diabetes mellitus.

Investigations for Diabetes Mellitus

Fasting and Postprandial Glucose:
- Fasting blood glucose (8-12 hours):
  - Normal: ≤110 mg/dl
  - Impaired glucose tolerance: 110-125 mg/dl
  - Diabetes mellitus: ≥126 mg/dl
- Two hours postprandial:
  - Normal: ≤140 mg/dl
  - Impaired glucose tolerance: 140-200 mg/dl
  - Diabetes mellitus: >200 mg/dl
Oral Glucose Tolerance Test (OGTT):
Glycosylated Hemoglobin (HbA1c):
- Normal:
  - Less than 5.7%
- Prediabetes:
  - 5.7% - 6.4%
- Diabetes:
  - Greater than 6.5%

Description

This quiz explores the mechanisms of blood glucose homeostasis, including the roles of diet, liver, skeletal muscle, and adipose tissue in regulating blood glucose levels. Understand how various hormones and digestive processes contribute to maintaining normal glucose ranges in the body.