Nutting Notes November 16

Growth hormone was once thought to be secreted constantly. Male rats have major periods of secretion. Episodic every 3 hours or so. Humans also have episodic secretion, less regular than rat. Ours when we go into deep sleep.
Finishing table of pituitary hormones- FSH and LH are gonadotropins. Sertoli cells promote spermatogenesis and follicular growth. Inhibin does not affect libido- inhibits FSH secretion.
Feeding vs. Fasting page:
Look from body’s perspective.
Objectives: The carbohydrates we eat fill out glycogen stores. Glycogen requires water, so we don’t store much glycogen. We lose glucose through kidneys if glucose in blood goes too high. TAG are stored. AAs may be used for gluconeogenesis, most stored as protein.
Reduction of gluconeogenesis and glycogenolysis results in an increase of glycogen stores.
Ketogenesis also declines when we eat. Insulin induces these things.
Between meals:
Need to keep up glucose for CNS. Muscle and other tissues burn fats for energy. Other sparable proteins can be broken down for gluconeogenesis.
FFA stands for free fatty acids (circulating, not esterified to glycerol).
Time-course of hormone action:
Primary mechanism by which short-acting hormones work- they change function of existing enzymes or transport proteins. They change enzyme activity or sensitivity to regulators.
Long acting hormones turn on mRNA and ribosomes to make more protein, mostly. Change amounts of enzymes.
Hormones in feeding vs. fasting
see chart
Big changes come from plasma insulin concentration and increase in anabolic processes. and decrease in catabolic processes, except glycolysis and TCA cycle.
Cortisol tends to try to keep glycogen steady, but effect is slight.
See chart for rest.
Between meals-see chart. If you fast many days, the levels of hormones that are otherwise constant will change.
High levels of GH or cortisol could exaggerate effects.
Lipolytic triggers are catecholamines.
Glucagon physiologically acts only in liver.
Insulin and Glucagon are from pancreas-see paper.
Figure 1, page 639, Johnson: Bulk of Islets are insulin-producing B cells. Somatostatin acts as a paracrine agent in these islets.
GIP gastric inhibitory peptide is now glucose-dependent insulinotropic peptide. Promotes response to glucose.
See figure 20 page 654- main stimulus of beta cells is glucose and amino acids. Inhibitory- somatostatin, epi, NE.
Permissive stimuli are GH, Cortisol. T3 increases sensitivity of beta cells to glucose and amino acids.
Glucagon secretion
3. Other stimuli- see text figure 19 page 653.
If you eat a low carbohydrate meal- insulin spikes. You become hypoglycemic without glucagon.
Normal meal: increased insulin, no change in glucagon. Liver may see more glucagon than peripheral tissue. Peripheral levels of glucagon do not change much. Liver uses it up.
Enough insulin gets past liver to affect muscle and fat cells.
Insulin stimulates glucose uptake . Utilization means oxidation or storage as glycogen or lipid.
Nerve cells require glucose, but insulin does not stimulate brain or nerve cells.
Glucose uptake- see figure 12 for how insulin signals transport of glucose receptors to membrane.
Glucagon actions:
promotes release from liver. Phosphorylase stim glycogen breakdown.
Decreases glycogen synthesis.
PK is pyruvate kinase.
Take home: glucagon influences activity of preformed enzymes to produce glucose from glycogen and spare glucose.
Actions of insulin:
most potent hormone.
Hormone-sensitive lipase is sensitive to catecholamines.
Last figure is intense. All the processes are shown together. Glycogen, fat, protein are the three storage forms. Insulin stimulates protein synthesis, amino acid uptake in muscle, inhibits protein breakdown in muscle. Glycogenesis increased by insulin. Insulin inhibits glycogen breakdown and decreases ability for catecholamines to stimulate glycogen breakdown. Glycolysis- insulin inhibits fat breakdown and stimulates lipogenesis. Catcholamines stimulate lipoysis and phopshorylase. Try to diagram out where all the previously listed things act.