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Download Diabetes and Exercise by Kenneth Cusi (auth.), Aristidis Veves, Kerry J. Stewart, PDF

By Kenneth Cusi (auth.), Aristidis Veves, Kerry J. Stewart, Jane E. B. Reusch, Judith G. Regensteinerr (eds.)

Diabetes is a big public illness within the usa. This assortment, Diabetes and Exercise, discusses the level of the matter of diabetes and sedentary way of life and offers a compelling reason for the significance of elevated actual task and workout in folks with diabetes. the concept that of workout as drugs has a powerful yet underappreciated medical foundation for the prevention and therapy of diabetes. Diabetes and Exercise, compiled through a staff of specialists within the field, specializes in either the physiological and functional facets of the valuable results of workout. This thorough collaboration presents the why's and how's to enforcing the actual job and workout adjustments so very important in diabetes prevention and sickness administration.

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LIP lipid infusion; SAL saline infusion. Data are means SE. 05 vs. 05 vs. 01 vs. control subjects. Adapted from Kashyap et al. (141). important feature determining the progression from normal glucose tolerance to overt hyperglycemia. If extended to the population at large, one may speculate that lipid-induced β-cell lipotoxicity may be the underlying mechanism for the observation that progression to T2DM is closely tied to the presence of obesity (251, 395, 396) and/or elevated plasma FFA (59, 395, 397), although other factors are likely to contribute to β-cell failure over time in T2DM.

Role Fatty Acids in the Control of Insulin Secretion In the fasting state, plasma FFA (not glucose) is the primary energy substrate for sustaining insulin secretion (378). Following a meal, pancreatic β-cells switch from using FFA to glucose as the preferred energy source. This occurs as glucose enters the β-cell by high-capacity, low-affinity GLUT2 The Epidemic of Type 2 Diabetes Mellitus 33 transporters and is rapidly phosphorylated to glucose-6-phosphate (G-6-P) by glucokinase that acts as the glucose sensor or “pacemaker” for insulin secretion (379).

Of note, both groups were well matched and subjects were lean and with no clinical features of the MS, having normal glucose tolerance, blood pressure, and plasma lipid profile. They were admitted twice to the clinical research center and received, in random order, a lipid or saline infusion. On days 1 and 2, insulin secretion was measured as part of a metabolic profile following mixed meals and in response to a +125 mg/dL hyperglycemic clamp (morning of day 3). Insulin action was examined on day 4 by the gold-standard euglycemic insulin clamp technique.

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