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USC BISC 307L - Thyroid and Growth Hormone II
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Control of Growth Hormone SecretionGrowth 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 growthIndirect effect by IGF circulating in tissueIndirect from liver IGF-1IGF-1 feedback and inhibit1. Strong age dependent pattern to growth hormone release (at hypothalamus)Post natal life mainlyAfter 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 life2. Circadian rhythm (hypothalamus)3. Fall in plasma glucoseFrom a high level (after a meal)Stimulates GH secretionPart of normal response to eatingEnergy being stored can be utilized to power tissue growthGrowth Hormone PathologiesDwarfismDeficiency in GH secretionOr deficiency in IGF receptorsIf in early childhood results in thisNot very common anymore because GH is available to treat deficienciesGigantism and acromegalyOver secretionWhen occurs in childhood- gigantismWhen occurs in adulthood- acromegalyMore difficult to treatBones 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 skinGestational Diabetes Mellitus1. Glucose intolerance (graph on slide illustrates this) is evident during pregnancy-normal in second half of pregnancy2. Some insulin resistance during pregnancy is normal-developed during pregnancySome women don’t show this at allNormally Beta cells increase insulin secretion to compensateIn response to insulin resistance the beta cells will secrete more insulinPlasma glucose may not elevate at all because this system worksOverworking beta cells may lead to type 2 diabetesWhat causes insulin resistance?1. Insulin resistance due to maternal adiposity2. Insulin resistance due to hormones from fetal placenta (human placental lactogen)progesterone-maintains enlarged uterushuman placental lactogen (hPL)hPL helps ensure adequate glucose supply for fetusinterferes with the action of insulinfetus wants more glucose so messes with endocrine systemevolutionary considerationsyou would think that the mother and the fetus both should survivethat’s not the way it is because they don’t have the same interestsmother is only 50% interested in passing on genes but fetus is 100% interested in passing on its own genesso 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 timestresses out the mother’s pancreas so if mother has diabetic or pre-diabetic risk then this pushes them over the edgemakes 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 oddsCalcium BalanceCalcium in the BodyRolesAs calcium phosphate (hydroxyapatite): 99%Forms the mineral portion of bonesStorage pool of calciumAs Ca2+: 1%Intracellular signal for enzymes, contraction, exocytosis etcNecessary for adhesion at tight junctionsCofactor for blood coagulationAffects neuronal excitability (hypocalcemia(low calcium in blood)hyperexcitability(nerves get really excited)Hormones that Regulate Body CalciumCome from two main places1. Thyroid and parathyroid glandsC cellsParathyroid hormone2. Vitamin Dnecessary component of dietmade in our skin in response to sunlightBISC 307L 1st Edition Lecture 18 Current Lecture- Control of Growth Hormone Secretionoo Growth hormone secretion from somatotrophs of APDirectly stimulated byGHRH 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-1o IGF-1 feedback and inhibito 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 Pathologieso 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 Mellituso 1. Glucose intolerance (graph on slide illustrates this) is evident during pregnancy-normal in second half of pregnancyo 2. Some insulin resistance during pregnancy is normal-developed during pregnancyo 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 diabeteso 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 systemo 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-


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USC BISC 307L - Thyroid and Growth Hormone II

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