Ways to make ATPInsulinPhysiology 206 1STedition Lecture 33Outline of Last Lecture I. Hypothyroidism II. HyperthyroidismOutline of Current Lecture I. GlucocorticoidII. AldosteroneIII. Adrenal MedullaIV. InsulinV. DiabetesCurrent LectureGlucocorticoid- Cortisol Stimulates liver to produce glucose from amino acids Stimulates the breakdown into amino acids from protein Increase plasma levels of glucose and amino acids go up; while protein goes down. Inhibits glucose uptake- except in brain Fat mobilization- use this as a fuel Permissive effects- almost every hormone that have effects has to have a little Cortisol Extremely important for body to deal with stress  Anti-inflammatory and immunosuppressive- reduces it, but not at a physiological level ~ Secretion under control of Pituitary; secretes when Pituitary releases ACTH. also stimulates hypertrophy with high levels of ACTH ~ ACTH is stimulated by the Hypothalamus, which releases CRH ~ Cortisol inhibits ACTH and LRH; Feedback SystemThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.Too Much- Hyper levels of Aldosterone: Blood Pressure goes up Sodium level goes up Potassium level goes down usually caused by Aldosterone secreting tumor.- Hyper levels of Cortisol: called Cushing's Syndrome Elevated blood glucose levels Protein loss- muscle weakness and loss Development of fatty deposits usually in face (moon face) Protein loss causes patient much less able to heal wounds because ability to make collagen decreases- Hyper levels of DHEA: has no effect in men because they have so much testosterone In women:1.) Hirsutism- develop facial hair2.) Pattern of hair growth is more masculine3.) Develop other male characteristic (body muscles)4.) Depress secretion of female hormones:a.) decrease breast sizeb.) causes menstruation problems  Young boys do not have testosterone, so if they have hypersecretion of DHEA, they have Precocious Puberty- artificial puberty. Grow hair and voice changes, but do not start producing sperm.Inadequate Amounts- Addison's Disease- Adrenal Cortex Atrophy reduced levels of all adrenal cortical hormones reduced Cortisol doesn't allow good stress management causes hypoglycemia- tired all the time; headaches lives not threatened reduced levels of Aldosterone is life threatening due to large amount of sodium, which causes loss of blood, which causes shock. Pretty easy to treat- high salt diet or medications Untreated will die in about a weekAdrenal Medulla- Inside Adrenal Cortex where releases noroepinephrine  Part of the Sympathetic Nervous System- begin in CNS; preganglionic neuron forms synapes forms ganglion and then post ganglionic neuron projects to target cell. cells are basically post ganglionic cells, but they release transmitters directly into target; release epinephrine Epinephrine is very similar to noroepinephrine these cells synthesize 4 times as much Epinphrine as noroepinphrine; 80% epi to 20% noro Store in granules- they stain very easily, called Chromaffin Granules Cells of Adrenal Medulla called Chromaffin Cells Effects of Epinephrine is very similar to Noroepinephrine Noro and epi have different receptors- Important Effects: make stimulation last longer mobilizes stored carbos and fat stimulates synthesis of glucose there is no such thing as disorder of lacking adrenal medulla parasympathetic would take care of loss. Was originally called Adrenaline.- Pheochromocytoma- tumor that releases epinephrine and noroepinephrine spontaneously chronic high levels Rapid Pulse High BP High blood glucoseGeneral Rule: able to synthesize lower level precursors of fat, carbohydrates, proteins to each other.Ways to make ATP- Major Producers:1.) glucose2.) glycerol3.) fatty acid- Stored as glycogen in glucose- Fatty acid glycerol stored as fat- Not much storage of glycogen- Lots of storage of fat- Glucose is the only thing that the brain can use as fuel Reason why the blood glucose regulated closely; blood glucose = 100mg/dL; 100mg%; 1 mg/mL Reason we regulate, is that we switch metabolism, in everything except in brain, to fat as fuel.Gluconeogensis- conversion of other things into glucose- Because we eat periodically instead of constantly, we have 2 separate metabolisms:1.) Fed = Absorptive State2.) Starving = Postabsorptive State  These exist at different times  When in Absorptive State, absorbing digested food, during state burning glucose as fuel everyone here.  Postabsorptive- not absorbing digested food, during state, burning fattry acids, except in brain.  These flip flop back and forth  Which one of these states that a person is in is controlled by Endocrine System  Epinephrine, Cortisol, growth hormone have effects on the control  The Dominant control:Islets of Langerhaus (Pancreatic Islets)- endocrine organ in pancreas- 2 Hormones Produced:1.) Beta- Insulin2.) Alpha- Glucagan  The balance between these two determine which metabolic state person is in.Insulin- Created by beta hormones; released into blood stream, NOT pancreatic duct- Promotes the conversion of glucose to glycogen in liver and muscle- Promotes uptake of fatty acid- Promotes uptake of amino acids - Promotes these conversions to glucose- Promotes uptake of glucose- Reduce level of fatty acids- Reduce level of amino- Reduce level of glucose in plasma- Increase glucose levels in cells- Convert amino acid in glucose increase glucose in cells- Convert fatty acid in glucose increase glucose in cells- Increase the amount of glycogen stored- Inhibits glycogen breakdown- In presence of elevated insulin removing nutrients from plasma, storing glycogen- Does this when digested food is being absorbed- Major stimulus is elevated blood glucose levels- When Insulin goes up, liver and muscles take up fatty acids, inhibit breakdown of glycogen- Neural control also factors into control: sympathetic fibers that terminate on Islets of Langerhaus, and inhibits secretion of insulin parasympathetic stimulates insulin secretion when digesting meal, parasympathetic stimulation is high Reason tired after a meal because blood is being reduced elsewhere, and taken to gut.Diabetes Insipidous- ADH deficiency, tasteless urine producedDiabetes Mellitus- means