Introduction:
In a healthy adult, the normal blood glucose concentration ranges between 70–99 mg/dL (fasting) and rises up to 140 mg/dL after meals (postprandial). Even slight deviations from this normal range can lead to hyperglycemia (high blood sugar) or hypoglycemia (low blood sugar).
The body maintains blood glucose within this narrow range through the coordinated actions of several hormones. The hormonal regulation of carbohydrate metabolism is achieved by internal chemical messengers, primarily:
- Insulin
- Glucagon
- Epinephrine (Adrenaline)
- Cortisol
- Growth Hormone (GH)
- Thyroid Hormones (T₃ and T₄)
Insulin:
Insulin is a peptide hormone secreted by the β-cells of the islets of Langerhans in the pancreas. It is released in response to elevated blood glucose levels and promotes anabolic (energy-storing) processes, thus helping maintain normal glucose balance.
Effects of Insulin:
- General Effect: Lowers blood glucose levels by promoting glucose uptake into cells via GLUT-4 transporters (especially in muscle and adipose tissue).
- Adipose Tissue:
- Increases fatty acid and triglyceride synthesis.
- Decreases lipolysis (fat breakdown).
- Liver and Muscle:
- Increases glycogen synthesis (glycogenesis).
- Decreases glycogen breakdown (glycogenolysis).
Glucagon
Glucagon is also a peptide hormone, secreted by the α-cells of the pancreas. It acts as an antagonist to insulin and performs catabolic functions. Glucagon is released when blood glucose levels fall below normal, helping restore glucose homeostasis.
Effects of Glucagon:
- In the Liver:
- Stimulates glycogen breakdown (glycogenolysis).
- Promotes glucose synthesis from non-carbohydrate sources (gluconeogenesis).
- Enhances ketone body formation (ketogenesis).
- Inhibits glycogen synthesis.
- In Muscles:
- Increases protein degradation.
- Decreases protein synthesis.
- In Adipose Tissue:
- Increases fat breakdown (lipolysis).
- Decreases triglyceride synthesis.
Overall effect: Glucagon raises blood glucose levels by mobilizing stored glycogen and fat while promoting ketone body utilization.
Catecholamines (Epinephrine and Norepinephrine)
Catecholamines are stress hormones produced by the adrenal medulla and nerve tissues. They play a crucial role in the body’s “fight-or-flight” response and rapidly increase blood glucose during emergencies or stress.
Epinephrine (Adrenaline)
Epinephrine is secreted by the adrenal medulla during physical or emotional stress and acts as a powerful antagonist to insulin. It helps the body meet energy demands by mobilizing glucose and fatty acids.
Effects of Epinephrine:
- Liver:
- Increases glycogenolysis.
- Promotes gluconeogenesis.
- Inhibits glycogen synthesis.
- Adipose Tissue: Enhances lipolysis, releasing fatty acids for energy.
- Skeletal Muscle: Stimulates glycogenolysis to supply glucose for muscle contraction.
Overall, epinephrine increases blood glucose levels and inhibits insulin secretion while stimulating glucagon release.
Glucocorticoids (Cortisol)
Cortisol is the main glucocorticoid hormone produced by the adrenal cortex. It acts slowly but has prolonged effects, especially during chronic stress, by increasing glucose availability for the body’s energy needs.
Effects of Cortisol:
- In Muscles:
- Increases protein breakdown (proteolysis).
- Decreases protein synthesis.
- In the Liver:
- Enhances gluconeogenesis (glucose production from amino acids).
- Promotes glycogen breakdown.
- In Adipose Tissue: Increases lipolysis, releasing free fatty acids for energy.
Overall effect: Cortisol supports glucose production and fat utilization during stress, acting as an insulin antagonist.
Growth Hormone (GH)
Growth hormone is secreted by the somatotrophic cells of the anterior pituitary gland. Its release is stimulated when blood glucose levels fall, plasma fatty acid levels are low, or plasma amino acid levels rise. It also increases during sleep, exercise, and stress.
Regulation of GH Secretion:
Growth hormone secretion is controlled by three hormones:
- Growth Hormone-Releasing Hormone (GHRH) – stimulates GH release.
- Somatostatin – inhibits GH release.
- Ghrelin – enhances GH secretion (produced in the stomach).
Effects of Growth Hormone:
- Increases plasma glucose, fatty acid, and glycerol levels.
- Inhibits glucose uptake by adipose and muscle tissue.
- Increases lipolysis in adipose tissue, releasing free fatty acids for energy.
- Stimulates gluconeogenesis and glycogenolysis in the liver.
Thyroid Hormones (T₃ and T₄)
Thyroid hormones (T₃ and T₄) are iodinated derivatives of tyrosine, secreted by the thyroid gland under the influence of thyroid-stimulating hormone (TSH) from the pituitary gland. The normal serum range is 5–12 µg/dL.
Hyperthyroidism (excess T₃/T₄) increases metabolism and blood glucose, whereas hypothyroidism (deficiency) lowers metabolic rate and blood glucose.
Effects of Thyroid Hormones:
- In Hyperthyroidism:
- Increases glycogenolysis and gluconeogenesis.
- Enhances lipolysis and ketone body synthesis.
- Promotes breakdown of muscle proteins.
- Raises blood glucose levels (catabolic effect).
- In Hypothyroidism:
- Decreases blood glucose by promoting glycogenesis.
- Increases protein synthesis (anabolic effect).
Summary Table: Hormonal Effects on Blood Glucose
| Hormone | Main Source | Effect on Blood Glucose | Primary Action |
|---|---|---|---|
| Insulin | β-cells of pancreas | Decreases | Promotes glucose uptake and storage |
| Glucagon | α-cells of pancreas | Increases | Stimulates glycogenolysis and gluconeogenesis |
| Epinephrine | Adrenal medulla | Increases | Activates glycogen breakdown and lipolysis |
| Cortisol | Adrenal cortex | Increases | Promotes gluconeogenesis and fat mobilization |
| Growth Hormone | Anterior pituitary | Increases | Stimulates gluconeogenesis and inhibits glucose uptake |
| Thyroid Hormones (T₃, T₄) | Thyroid gland | Varies (↑ in hyperthyroidism, ↓ in hypothyroidism) | Regulates metabolic rate and energy balance |
Detailed Notes:
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