7.3 Animal Hormones and Blood-Glucose Control

Blood glucose normally fluctuates within a regulated range as glucose enters from the intestine, is used in respiration, stored or released. Pancreatic β cells detect rising glucose and secrete insulin. Insulin promotes glucose uptake in responsive muscle and adipose tissue, glycogen synthesis in liver and muscle, and other storage pathways. These effects lower the deviation and reduce further insulin stimulation.

When glucose falls, pancreatic α cells secrete glucagon. In liver, glucagon promotes glycogen breakdown and formation of glucose from non-carbohydrate substrates, increasing glucose release into blood. Insulin and glucagon are antagonistic because their overall effects oppose one another. Negative feedback does not hold glucose at one unchanging number; it limits departures while demand, meals and activity continue to vary.

Type 1 diabetes results from autoimmune destruction of pancreatic β cells, leading to severe insulin deficiency. Without treatment, glucose uptake and storage are impaired, blood glucose rises and glucose may appear in urine. Its osmotic effect increases urine production, producing dehydration and thirst. Cells also shift metabolism, and dangerous ketoacidosis can develop. Insulin replacement and glucose monitoring are essential.

Type 2 diabetes begins mainly with insulin resistance: target tissues respond inadequately even though insulin is produced, and β cells may initially compensate with greater secretion. Over time β-cell function can decline. Genetic predisposition, age, adipose-tissue biology, diet and physical activity influence risk. Calling it simply a lifestyle disease is biologically incomplete and can encourage stigma; modifiable risks interact with inherited and environmental factors.

Persistent high glucose damages blood vessels and tissues, increasing risks to retina, kidney, nerves and cardiovascular system. Management may include dietary pattern, exercise, weight management where appropriate, oral medicines, injected receptor agonists or insulin, depending on disease and individual needs. Continuous glucose monitors measure interstitial glucose and reveal trends, while insulin pumps can automate part of delivery; neither removes the need for feedback-informed decisions.

A statistical association between a hormone concentration and disease could arise because the hormone affects disease, disease affects the hormone, or another factor affects both. Stronger causal inference can come from longitudinal data, interventions, mechanistic evidence and genetic variants that alter exposure. Large sample size narrows random uncertainty but does not automatically remove confounding or reverse causation.