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Figure 11-5

(secondary hyperaldosteronism), which may occur with renin-producing juxtaglomerular cell tumors or other kind of renal disorders. There are fluid retention, hypertension, and potassium loss (hypokalemia) with associated muscle weakness. Aldosterone, in addition to promoting potassium exchange for sodium, also promotes exchange of H+ for sodium. Hence, hyperaldosteronism may also be associated with an alkalosis.

DEFICIENCY: May result from adrenal destruction. Moreover, since aldosterone secretion is stimulated both by ACTH and by angiotensin II, deficiency may result from either a decrease in ACTH or a deficiency of the renin-angiotensin system. There are fluid and sodium loss (perhaps even shock from decreased blood volume), and potassium elevation (hyperkalemia) with associated cardiac arrhythmias.

INSULIN: ORIGIN: Beta cells of pancreas STRUCTURE: Polypeptide

REGULATION: Secretion is stimulated by increased blood glucose concentration. An excess of certain amino acids also stimulates insulin secretion, which in turn clears the blood of excess amino acids by promoting the entry of certain amino acids into cells.

FUNCTION: Facilitates the uptake of blood glucose by cells for storage as glycogen (particularly in the liver and muscle); synthesis of protein (insulin also increases amino acid uptake by cells); synthesis of fatty acids in the liver, which are transported via VLDL lipoproteins to adipose cells, where they are stored as triglycerides. Or, the glucose may be utilized for energy or other cell functions. Insulin inhibits gluconeogenesis (formation of glucose). Insulin does not influence glucose uptake in the brain. Rather, glucose can enter brain cells without insulin. This is a good thing, as the brain requires glucose for fuel and would otherwise be terribly deprived if insulin levels were lacking; unlike other tissues, the brain cannot use fatty acids for fuel, as fatty acids do not cross the blood-brain barrier. That is why hypoglycemia is frequently accompanied by nervousness and even loss of consciousness.

EXCESS: Hypoglycemia (decreased blood glucose; nervousness, dizziness).

DEFICIENCY: Diabetes mellitus: elevated blood glucose, polyuria (increased urination), polydipsia (increased water intake), fatigue, coma, hyperlipemia.

Fig. 11-6. The effects of insulin on energy utilization. The presence or absence of insulin helps to decide

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