High glucose intake

A temporary rise in plasma glucose concentration immediately follows a meal, but within 2-3 hours the level returns to the preprandial level. Several factors influence the blood glucose profile. 

The rise in blood glucose level is quickly followed by a rise in the blood insulin level which increases three-to tenfold. An elevated blood glucose level directly stimulates pancreatic insulin release, as do leucine and arginine derived from digestion of protein. 

Release of gastrin, cholecystokinin, gastric inhibitory peptide, and glicentin appears to stimulate insulin release in an anticipatory manner in addition to regulating other digestive responses. 

Concomitant with insulin release are changes in glucagon release, whose magnitude and direction 

Hepatic glycogen synthesis after a meal. The permeability of the liver to glucose provides the substrate for hepatic glycogen synthesis. This synthesis is controlled by (1) activation of glycogen synthase by insulin, 

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The disposition of a high glucose intake is presented in Figure 22-11. 

Disposition of high glucose intake. FA, Fatty acid TG, triacylglycerol VLDL, very-low-density lipoprotein LDL, low-density lipoprotein. 

Chromium is a trivalent cption that occurs as A typical daily intake isO-5 3-8 jimoJ (25-200 ig/day). After absorption from the diet, chromium occurs bound to transferrin. A safe and adequate intake of 50 to 200 ffg Cr/day has been established. Chromium appears to participate in glucose metabolism. The ion may play a part in mediating the hormonal effects of insulin. Chromium deficiency results in abnormally high glucose tolerance curves and impaired clearance of plasma glucose. Chromium deficiency can be induced in animals. There is evidence that... 

HDI]), (2) deficient AVP action on the kidney (neplirogenic diabetes insipidus [NDI]), and (3) excessive water intake (psychogenic polydipsia). An osmotic diuresis may also produce polyuria and polydipsia. Uncontrolled diabetes mellitus with a high glucose load to the kidney is a common cause of an osmotic diuresis. 

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). 

However, most patients are not sufficiently predictable in their schedule and food intake to allow tight glucose control with this approach. If the fasting glucose in the morning is too high, the evening NPH dose may be moved to bedtime (now three total injections per day). This may provide sufficient intensification of therapy for some patients. 

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