Master Peptide Hormones with Picmonic for Medicine

Peptide hormones act within seconds to minutes because they work through signaling cascades rather than gene transcription. Because they bind only to the cell surface and affect change through secondary messengers, peptide hormones can cause the intended change in physiology relatively rapidly. The effects of peptide hormones are short-lived because they only temporarily induce secondary messengers, but do not affect long-term processes like translation or transcription.

Being hydrophilic, peptide hormones dissolve easily in plasma and circulate without carrier proteins. This contrasts with steroid and thyroid hormones, which are lipophilic and protein-bound.

They cannot cross the lipid bilayer, so they bind to receptors on the cell surface (e.g., GPCRs or receptor tyrosine kinases) rather than on intracellular receptors.

Signal transduction occurs via intracellular second messengers such as cAMP, IP3/DAG, calcium, or JAK/STAT pathways. This amplification allows small amounts of hormone to generate large effects.

Peptide hormones are derived from many amino acids and are processed in the endoplasmic reticulum. Peptide hormones are synthesized in the rough ER as preprohormones are derived from many amino acids, cleaved to prohormones, packaged into vesicles, and stored until secretion.

Oxytocin is a peptide hormone and a neuropeptide. It functions to allow the milk-letdown reflex and stimulates breastfeeding. Additionally, it increases uterine contraction. It also has functions in selective social bonding and sexual pleasure.

Secreted by the anterior pituitary. Stimulates growth and metabolism via the JAK/STAT pathway. Increases IGF-1 (somatomedin C) from the liver, promotes protein synthesis, and increases lipolysis. Excess GH will cause acromegaly/gigantism, while deficiency causes growth failure.

Insulin is a peptide hormone produced by the beta cells of the pancreas. It promotes glucose uptake from the bloodstream into muscle and adipose tissue via GLUT-4 translocation. In the liver and pancreatic β-cells, glucose transport occurs through GLUT-2, which is insulin-independent, but insulin enhances hepatic glucose utilization and storage by stimulating glycogen synthesis and inhibiting gluconeogenesis. Insulin also promotes lipogenesis and protein synthesis while inhibiting lipolysis. Deficiency of insulin or resistance to its effects leads to diabetes mellitus.

Secreted by thyroid parafollicular C cells when calcium is high. Inhibits osteoclast bone resorption to lower serum calcium. Not essential for calcium homeostasis, but high-yield in medullary thyroid carcinoma (tumor marker).

Secreted by the anterior pituitary. Stimulates milk production and breast development. Its secretion is inhibited by dopamine and increased by TRH. Hyperprolactinemia suppresses GnRH, leading to infertility, galactorrhea, and amenorrhea.

Released from pancreatic α-cells during hypoglycemia. Acts via cAMP (Gs receptor). Stimulates glycogenolysis, gluconeogenesis, lipolysis, and ketone production. Opposes insulin.

Secreted by parathyroid glands when calcium is low. Increases osteoclast activity (indirectly via osteoblasts), increases renal calcium reabsorption, decreases phosphate reabsorption, and activates 1-α hydroxylase to increase calcitriol (vitamin D).

Vasopressin, which is also called antidiuretic hormone, is released from the posterior pituitary during hyperosmolar states or hypovolemia. It acts on V2 receptors in the kidney collecting ducts to insert aquaporin-2 channels, promoting water reabsorption, and on V1 receptors to cause vasoconstriction. Deficiency results in central diabetes insipidus, while resistance at the level of the kidney causes nephrogenic diabetes insipidus.