Endocrine Systems Regulating Energy (Chapter 17)

A vocabulary-style set of flashcards covering key terms related to glucose and energy regulation by the endocrine system from the lecture notes.

Glucose homeostasis

The regulation of blood glucose levels by hormones (insulin, glucagon, cortisol) and the liver, muscle, and adipose tissues to maintain a narrow range.

Insulin

Peptide hormone from pancreatic beta cells that lowers blood glucose by promoting uptake and storage of glucose and inhibiting hepatic glucose production.

Glucagon

Peptide hormone from pancreatic alpha cells that raises blood glucose by stimulating glycogenolysis and gluconeogenesis in the liver.

Cortisol

Long-acting glucocorticoid steroid from the adrenal cortex that increases blood glucose via gluconeogenesis and promotes lipolysis and protein breakdown; also anti-inflammatory.

Pancreatic islets

Endocrine cell clusters in the pancreas that regulate glucose; include alpha and beta cells.

Alpha cells

Pancreatic islet cells that secrete glucagon.

Beta cells

Pancreatic islet cells that secrete insulin.

GLUT transporters

Glucose transporter proteins in cell membranes that mediate glucose entry into cells, essential for insulin-stimulated uptake.

Glycogenolysis

Breakdown of glycogen to glucose, primarily in liver and muscle.

Gluconeogenesis

Synthesis of glucose from non-carbohydrate sources (amino acids, lactate, glycerol) in the liver.

Glycogenesis

Formation of glycogen from glucose for storage in liver and muscle.

Lipolysis

Breakdown of triglycerides into glycerol and fatty acids in adipose tissue.

Lipogenesis

Formation of fatty acids and triglycerides for long-term energy storage.

Ketogenesis

Production of ketone bodies from fatty acids for use as alternate brain fuel during carbohydrate scarcity.

Ketones

Ketone bodies (e.g., acetoacetate, beta-hydroxybutyrate) used as energy sources when glucose is scarce.

Hyperglycemia

Elevated blood glucose levels.

Hypoglycemia

Low blood glucose levels.

AGEs (advanced glycation end-products)

Molecules formed when glucose glycates proteins/lipids, contributing to tissue stiffening and dysfunction.

Maillard reaction

Nonenzymatic reaction between reducing sugars and amino groups that forms AGEs.

Type I diabetes

Juvenile-onset diabetes due to autoimmune destruction of pancreatic beta cells, resulting in little/no insulin.

Type II diabetes

Diabetes characterized by insulin resistance and impaired insulin signaling; often associated with obesity.

Insulin receptor

Cell-surface receptor tyrosine kinase that mediates insulin signaling to promote glucose uptake and metabolism.

Negative feedback

Regulatory mechanism where the end product (e.g., cortisol) inhibits upstream hormones (CRH/ACTH) to maintain balance.

CRH (corticotropin-releasing hormone)

Hypothalamic hormone that stimulates pituitary ACTH release and initiates the cortisol axis.

ACTH (adrenocorticotropic hormone)

Pituitary hormone that stimulates the adrenal cortex to release cortisol.

Adrenal cortex

Outer layer of the adrenal gland that produces glucocorticoids (like cortisol).

Cushing syndrome

Condition of excess cortisol (often from tumors) causing edema and characteristic fat redistribution.

Addison’s disease

Adrenal insufficiency with low cortisol production.

Diurnal cortisol rhythm

Cortisol levels peak in the morning and decline during the day, part of the body’s daily cycle.