Negative feedback of blood glucose glucose is

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Negative Feedback of Blood Glucose Glucose is regulated by negative feedback to maintain tight control of levels. Insulin lowers glucose levels Glucagon raises glucose levels If glucose goes too low then brain cells can not function leading to unconsciousness. If glucose goes too high then damage to kidney, retina, peripheral nerves, cardiovascular system.
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The Pancreas α cells - release glucagon in response to low levels of glucose β cells - release insulin in response to high levels of glucose
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Glucose levels Brain needs a constant source of glucose Glycogen and triglycerides need to be broken down to glucose and fatty acids Liver can break down glycogen to glucose Liver can also break down amino acids (from muscles in the fasting state) to produce glucose This mechanism occurs primarily in the fasting state Regulation by other hormones (Fasting stage) Epinephrine – breaks down glycogen and triglycerides in liver Glucagon – released from pancreatic alpha cells; breaks down glycogen Glucocorticoids (i.e. cortisol)– breaks down glycogen
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Insulin receptors Cells in the body have glucose transporters which are activated via actions of insulin receptors Cells need insulin to activate their glucose transporters One exception is neurons which do NOT require insulin to utilize glucose
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Insulin inhibits AC/cAMP/PKA production by increasing cAMP phosphodiesterase (hormone that breaks down cAMP) and other diesterases to reduce phosyphorylation This inactivates hormone sensitive lipase to reduce lipolysis (i.e reduce the signal to burn fat) Insulin's actions at the insulin receptor are not fully understood Insulin causes: Glucose transport to muscles and fat Storage of glucose in the liver Inactivation of hormone sensitive lipase (reduce fat burning) Activation of acetyl Co-A carboxylase & Fatty acid synthase (induces storage of glucose into liver & adipose tissue)
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Interaction with ANS activity
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Blood Glucose Disorders: Diabetes Mellitus High glucose levels due to reduced insulin function results in kidney and liver damage, blindness. Type I “juvenile diabetes” or “insulin-dependent”. Genetic autoimmune disease affecting β cells Low insulin levels Treatable with insulin injections Type II “adult onset” or “insulin insensitive” Obesity related loss of insulin receptor function Normal or elevated insulin Treatable with drugs to enhance insulin receptor function.
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Figure 9.19 Incidence of obesity and type 2 diabetes is increasing worldwide among children
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New Type 1 treatments aimed at mimicking a healthy pancreas
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Type 2 Diabetes Glucose homeostasis in type 2 diabetes mellitus. Type 2 diabetes mellitus (T2DM) results from a combination of insulin resistance and inadequate insulin secretion (see the figure).
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