Endocrinology | Pancreas: Insulin Function

This paragraph introduces the pancreas as a heterocrine gland with both endocrine and exocrine functions. The endocrine part, particularly the islets of Langerhans, is composed of various cells including alpha and beta cells. Alpha cells secrete glucagon, which is released during low blood glucose levels (hypoglycemia), while beta cells secrete insulin, a hormone that responds to high blood glucose levels (hyperglycemia) by lowering them. The normal blood glucose range is specified as 80 to 120 milligrams per deciliter (mg/dL), with levels below 80 mg/dL indicating hypoglycemia and above 120 mg/dL indicating hyperglycemia.

The paragraph delves into the process of insulin production within beta cells. It describes the transcription of the insulin gene into mRNA, which then translates into preproinsulin in the ribosomes. This precursor undergoes modifications in the endoplasmic reticulum and Golgi apparatus, resulting in the formation of insulin and C-peptide within vesicles. The stimulus for insulin secretion is hyperglycemia, which triggers the uptake of glucose via the GLUT2 transporter, independent of insulin. The subsequent metabolic pathways involving glycolysis, the Krebs cycle, and the electron transport chain lead to the production of ATP. The increase in ATP closes potassium channels, leading to the accumulation of positive charges and the opening of calcium channels. The influx of calcium ions facilitates the fusion of insulin-containing vesicles with the cell membrane, releasing insulin, C-peptide, and amylin into the bloodstream.

This paragraph explains insulin's role in the liver, where it binds to tyrosine kinase receptors, activating intracellular messengers like PI3K and AKT (protein kinase B). These activations stimulate glycogenesis, the conversion of glucose into glycogen for storage, and glycolysis, the metabolic pathway converting glucose into pyruvate. Insulin's actions effectively lower blood glucose levels by promoting glucose uptake and utilization in the liver, which is crucial for maintaining energy homeostasis.

Insulin's effects on muscle tissue are highlighted, where it enhances glucose uptake by activating the GLUT4 transporter, a process dependent on insulin. The hormone also stimulates glycolysis and glycogenesis within muscle cells, promoting the conversion of glucose into pyruvate and glycogen, respectively. Additionally, insulin supports protein synthesis by facilitating the uptake of amino acids and their assembly into proteins, contributing to muscle growth and repair.

The paragraph discusses insulin's function in adipose tissue, where it stimulates glucose uptake through the GLUT4 transporter and promotes lipogenesis, the synthesis of fatty acids and triglycerides. Insulin aids in the conversion of dihydroxyacetone phosphate (DHAP) into glycerol and acetyl-CoA into fatty acids, which are then combined to form triglycerides. This process is crucial for energy storage and contributes to the regulation of blood glucose and lipid levels.

This concluding paragraph recaps insulin's diverse actions across the liver, muscle, and adipose tissue. It summarizes insulin's role in glucose uptake, glycolysis, glycogenesis, protein synthesis, and lipogenesis. The paragraph emphasizes the importance of insulin in maintaining blood glucose levels during the absorptive state after eating and foreshadows the discussion of diabetes, where insulin deficiency or resistance can lead to significant health complications.