BISC 307L 1st Edition Lecture 18 Current Lecture Control of Growth Hormone Secretion o o Growth hormone secretion from somatotrophs of AP Directly stimulated by GHRH and SS inhibits secretion from anterior pituitary GH affects indirectly by stimulating liver to secrete IGF 1 and directly by stimulating target cells results in 3 different Direct on stimulating growth Indirect effect by IGF circulating in tissue Indirect from liver IGF 1 o IGF 1 feedback and inhibit o 1 Strong age dependent pattern to growth hormone release at hypothalamus Post natal life mainly After birth GH secretion high in children and rises until puberty where is reaches its peak and start a slow steady decline for the rest of life o 2 Circadian rhythm hypothalamus o 3 Fall in plasma glucose From a high level after a meal Stimulates GH secretion Part of normal response to eating Energy being stored can be utilized to power tissue growth Growth Hormone Pathologies o Dwarfism Deficiency in GH secretion Or deficiency in IGF receptors If in early childhood results in this Not very common anymore because GH is available to treat deficiencies o Gigantism and acromegaly Over secretion When occurs in childhood gigantism When occurs in adulthood acromegaly More difficult to treat Bones grow in childhood and adolescence but when the tissues at the end of the long bones cease growing then elongation of bones no longer possible but bones can still grow in thickness causing a disfiguring condition and limits mobility and changes in skin Gestational Diabetes Mellitus o 1 Glucose intolerance graph on slide illustrates this is evident during pregnancy normal in second half of pregnancy o 2 Some insulin resistance during pregnancy is normal developed during pregnancy o Some women don t show this at all Normally Beta cells increase insulin secretion to compensate In response to insulin resistance the beta cells will secrete more insulin Plasma glucose may not elevate at all because this system works Overworking beta cells may lead to type 2 diabetes o What causes insulin resistance 1 Insulin resistance due to maternal adiposity 2 Insulin resistance due to hormones from fetal placenta human placental lactogen progesterone maintains enlarged uterus human placental lactogen hPL hPL helps ensure adequate glucose supply for fetus interferes with the action of insulin fetus wants more glucose so messes with endocrine system o evolutionary considerations you would think that the mother and the fetus both should survive that s not the way it is because they don t have the same interests mother is only 50 interested in passing on genes but fetus is 100 interested in passing on its own genes so there is conflict fetus messes with endocrine system to help itself with more glucose But mother just secretes more insulin more hPL and insulin being secreted at the same time stresses out the mother s pancreas so if mother has diabetic or pre diabetic risk then this pushes them over the edge makes sense because the mutation of the fetus will only pay the cost of evolving their mothers this way in only a fourth of their offspring and those are pretty good odds Calcium Balance Calcium in the Body o Roles As calcium phosphate hydroxyapatite 99 Forms the mineral portion of bones Storage pool of calcium As Ca2 1 Intracellular signal for enzymes contraction exocytosis etc Necessary for adhesion at tight junctions Cofactor for blood coagulation Affects neuronal excitability hypocalcemia low calcium in blood hyperexcitability nerves get really excited Hormones that Regulate Body Calcium o o Come from two main places 1 Thyroid and parathyroid glands C cells Parathyroid hormone 2 Vitamin D necessary component of diet made in our skin in response to sunlight
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