Diabetes mellitus, metabolic syndrome, gestational diabetes mellitus, adenohypophysis, neurohypophysis, diabetes insipidus, SIADH (syndrome of inappropriate ADH secretion), growth hormone, epiphyseal growth plate, achondroplasia, bone growth (periosteal)

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Biomedical Science
BMS 460
D.Rao Veeramachaneni

23 October Ramifications of Diabetes Mellitus: Metabolic Syndrome Combination of type 2 diabetes, atherosclerosis, and high blood pressure Criteria Central obesity Fasting blood glucose ≥ 110 md/dL Elevated fasting plasma triglycerides Low plasma HDL levels Blood pressure ≥ 130/85 mm Hg Renal disease is also associated now Obesity is not only an independent predictor of end-stage renal disease but is also correlated to albuminuria Metabolic syndrome may affect as high as 25% of the US population Obesity/diet, inactivity, genetic factors, lack of exercise, high calorie intake → altered malonyl-CoA/AMPK Adiponectin, leptin, TZDs, metformin inhibit altered malonyl-CoA/AMPK Altered malonyl-CoA/AMPK → hypertension, myopathies, diabetes, insulin resistance, dyslipidemia, atherosclerosis, CVD, NAFLD/NASH Drug Targets for Type 2 DM Stimulate beta cell secretion of insulin Slow digestion or absorption of carbohydrates Inhibit hepatic glucose output Make target tissues more responsive to insulin Gestational Diabetes Mellitus Any degree of glucose intolerance that develops during pregnancy due to inability to secrete adequate insulin to overcome insulin resistance created by placental hormones Pregnancy is a counter regulatory state with elevation of multiple blood glucose- elevating hormones GDM occurs because of insulin resistance as well as inability of the pancreas to make the additional insulin that is needed to support the placenta. Precipitated by the increasing levels of hormones such as chorionic somatomammotropin (placental lactogen), progesterone, cortisol, and prolactin all of which have counter-regulatory anti-insulin effects If untreated, gestational diabetes, or even poorly controlled type 1 or type 2 diabetes in a pregnant woman, can lead to Fetal macrosomia (abnormally large body size) Neonatal hypoglycemia because of pancreatic hyperplasia and excess insulin secretion Also, hypocalcemia, polycythemia and hyperbilirubinemia in the newborn Results in jaundice, require phototherapy Complications for the mother including a greater risk for chronic hypertension and cesarean delivery Genetic predisposition to disease that might otherwise remain latent for decades may be manifested first – often transiently – during pregnancy Many individuals who go on to manifest type 2 DM later in life first manifest the disease during pregnancy High maternal blood glucose triggers increased insulin secretion by fetus → altered fetal islet function → child obesity, pubertal impaired glucose tolerance → impaired adult islet function Parvocellular system: nuclei sending axons to median eminence Secretes hormones to affect hypothalamic-pituitary portal vessels Adenohypophysis Acidophils (somatotrophs and lactotrophs) secrete two major peptide hormones: growth hormone and prolactin Basophils (gonadotrophs, thyrotrophs, and corticotrophs) secrete glycoprotein hormones: the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH), thyroid-stimulating hormone (TSH), and adrenocorticotropic hormone (ACTH), or corticotropin Chromophobes include cells that have depleted their hormone context and lost the staining affinity typical of acidophils and basophils Endocrine cells are precisely identified by immunohistochemistry Use antibody to tag specific sort of cell Neurohypophysis The neurohypophysis is formed by supporting neuroglial cells – the pituicytes – which surround the unmyelinated nerve fibers arising from paraventricular (PVN) and supraoptic (SON) nuclei. Vasculature is abundant. PVN primarily secretes oxytocin and SON primarily secretes anti-diuretic hormone (ADH, also called arginine vasopressin) These hormones are transported along the axons together with the carrier protein neurophysin and accumulate in axon dilations called Herring bodies When released at axon terminals, they enter fenestrated capillaries derived from inferior hypophyseal artery Diabetes Insipidus: ADH Deficiency Normally, ADH binds to a vasopressin II receptor on the collecting duct cells, causing a cAMP-mediated translocation of aquaporin-2 to the apical surface of the cell. Aquaporins increase the permeability to water. In the absence of ADH, water cannot be reabsorbed normally to correct hyperosmolarity, and hypernatremia (high levels of Na in plasma), polyuria (excessive volume of urine and frequency of urination), and polydipsia (thirst and increasing drinking) occur Central or nephrogenic Central diabetes insipidus Tumors Trauma Surgery Lead to ADH deficiency Nephrogenic diabetes insipidus Renal disease ADH-unresponsive kidney Drugs (lithium) Alcohol inhibits release of ADH from SON. Also acts as an antagonist for ADH in the kidneys, which prevents aquaporins from binding to the collecting ducts Pregnancy: placenta secretes vasopressinase resulting in features of both central and nephrogenic DI. Normally its plasma level falls after delivery. Treat with synthetic anti-diuretic hormone SIADH, the Syndrome of Inappropriate ADH secretion SIADH is the opposite of diabetes insipidus Patients with SIADH secrete inappropriately high levels of ADH (i.e., arginine vasopressin [AVP]) or AVP-like substances Thus, the urine osmolality is inappropriately high as the kidney salvage inappropriately large volumes of water from the urine As a result, total body water increases, the blood becomes hypo-osmolar, and plasma [Na ] drops (hyponatriema) Hyponatremia: two mechanisms Dilution of plasma Increased excretion of sodium by the kidneys Sodium excretion is increased because of the expanded plasma volume, which enhances sodium filtration and reduces sodium reabsorption Excessive ADH secretion → increased water reabsorption by renal tubule → dilutional hyponatremia, increased plasma volume Dilutional hyponatremia → hyponatremia Increased plasma volume → ↓ aldosterone secretion, ↑ glomerular filtration rate ↓ aldosterone secretion → ↓ sodium reabsorption → increased sodium excretion ↑ glomerular filtration rate → ↑ sodium filtration → increased sodium excretion Increased sodium excretion → hyponatremia Major known hypophysiotropic hormones Major effect on anterior pituitary Corticotropin-releasing hormone (CRH) Stimulate secretion of ACTH Thyrotropin-releasing hormone (TRH) Stimulates secretion of TSH Growth hormone-releasing hormone (GHRH) Stimulates secretion of GH Somatostatin (SS) Inhibits secretion of GH Gonadotropin-releasing hormone (GnRH) Stimulates secretion of LH and FSH Dopamine (DA) Inhibits secretion of prolactin FSH and LH → gonads Germ cell development Female → ovum Male → sperm Secrete hormones Female → estradiol, progesterone Male → testosterone Growth hormone →
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