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Down-regulates glycogen synthase activity
4%
5/131
Up-regulates glycogen phosphorylase activity
11%
15/131
Enhances potassium uptake
75%
98/131
Downregulates HMG-CoA reductase
3%
4/131
Crosses the placenta to affect the fetus
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This patient's clinical presentation is highly suggestive of type I diabetes mellitus considering the low BMI, increased thirst/urination and high blood glucose. The deficient hormone is insulin, which has the ability to enhance potassium uptake into cells. Type I diabetes mellitus (TIDM) is characterized by destruction of the beta islet cells of the pancreas. This is accomplished by an autoimmune process. T1DM seems to occur in genetically susceptible individuals, with environmental factors precipitating the event. Because there is inadequate insulin secretion secondary to pancreatic beta cell destruction, these patients are said to be insulin dependent. Insulin plays a crucial role in increasing glucose transport into adipocytes and skeletal muscle. Insulin also increases the synthesis of triglycerides and glycogen. Insulin has the ability to shift potassium into cells. In fact, insulin can be used in the management of patients presenting with signs and symptoms of hyperkalemia. Incorrect Answers: Answer 1: Down-regulation of glycogen synthase is incorrect. Insulin upregulates this enzyme's activity. Answer 2: Up-regulation of glycogen phosphorylase is incorrect. Insulin does the opposite, as it promotes glycogen synthesis. Glycogen phosphorylase is involved in glycogen breakdown. Answer 4: Insulin upregulates HMG-CoA reductase, the rate limiting step of cholesterol synthesis. Answer 5: Insulin is unable to cross the placenta and affect the fetus.
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