Hypoglycemia in Diabetes: Pathophysiology, Prevalence, and by Philip E. Cryer M.D.

By Philip E. Cryer M.D.

Iatrogenic hypoglycemia, or low blood glucose attributable to scientific remedy, is a problem dealing with individuals with diabetes and their overall healthiness care services. Philip E. Cryer, MD—a Banting Medal recipient and the Irene E. & Michael M. Karl Professor of Endocrinology and Metabolism at Washington college in St. Louis—examines this continual challenge from a pathophysiological perspective.

Intended for diabetes researchers and doctors who paintings heavily with sufferers with diabetes, Hypoglycemia in Diabetes offers direct perception into the explanations and effects of this severe scientific from one of many most suitable specialists within the box. in response to the newest advancements and developments within the medical and clinical literature, readers are given the main points they want that allows you to be told approximately how you can determine, hinder, and deal with this unlucky situation of the diabetes care regimen.

The moment version comprises up to date and multiplied references from the most recent learn. The dialogue of iatrogenic hypoglycemia has been improved all through to hide those new findings and to maintain the dialogue of the subject suitable.

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2010) and blood-to-brain lactate transport increases when plasma lactate levels are raised to very high concentrations by vigorous exercise (Dalsgaard 2006) or by lactate infusion coupled with exercise (van Hall et al. 2009). It is thought that such lactate oxidation might support 5 to 10% of neuronal metabolic needs (Herzog et al. 2011). 38 Interestingly, in a study employing 13C nuclear magnetic resonance spectroscopy during [13C]glucose infusion in eight healthy humans, van de Ven et al. -1 respectively.

As discussed later in this chapter, a decrease in insulin is the first physiological defense against hypoglycemia (Cryer 2001, 2008). Glucagon Glucagon secretion is stimulated by low glucose, amino acids, β2-adrenergic activation by catecholamines such as epinephrine and norepinephrine, acetylcholine released from parasympathetic nerves, and glucose-dependent insulinotropic polypeptide; it is inhibited by high glucose, insulin, nonesterified fatty acids, somatostatin, and glucagon-like peptide-1 (Cryer 2001, 2008, 2010, 2011a; Cherrington 2001).

C-peptide is co-secreted with insulin but not cleared by the liver. Insulin secretion so calculated virtually ceases during hypoglycemia in humans (Heller and Cryer 1991a). The physiology of insulin action has been reviewed (Ferrannini 2012). Insulin suppresses hepatic glycogenolysis rapidly and hepatic (and renal) gluconeogenesis more gradually and thus suppresses endogenous glucose production (Cryer 2001, 2008, 2010, 2011a; Cherrington 2001; Edgerton et al. 2006). Basal insulin levels restrain glucose production in the postabsorptive state, and increased insulin levels suppress glucose production and stimulate glucose utilization in the postprandial state.

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