By Philip E. Cryer M.D.
Intended for diabetes researchers and doctors who paintings heavily with sufferers with diabetes, Hypoglycemia in Diabetes presents direct perception into the reasons and results of this critical clinical situation from one of many premier specialists within the box. in keeping with the most recent advancements and traits within the medical and clinical literature, readers are given the main points they want so one can learn approximately the way to determine, hinder, and deal with this unlucky condition of the diabetes care regimen.
The moment version comprises up to date and elevated references from the most recent learn. The dialogue of iatrogenic hypoglycemia has been elevated all through to hide those new findings and to maintain the dialogue of the subject correct.
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Additional info for Hypoglycemia in Diabetes: Pathophysiology, Prevalence, and Prevention
In reality, that is sometimes not practical and it is often not done. Nonetheless, it could be reasoned that the detrimental effects of brief erroneous treatment for suspected hypoglycemia are less than those of failure to treat an episode of bona fide hypoglycemia (Cryer 2007). Symptoms Symptoms of hypoglycemia are categorized as neuroglycopenic—those that are the direct result of brain glucose deprivation per se—and neurogenic (or autonomic)—those that are largely the result of the perception of physiological changes caused by the central nervous system (CNS)–mediated sympathoadrenal discharge triggered by hypoglycemia (Cryer 2007, 2008, 2010, 2011a; Schwartz et al.
Neurons normally oxidize lactate as well as glucose, but that is largely lactate derived from glucose within the brain—mostly glucose transported from the circulation into the brain but partly that derived from glycogen in astrocytes (Itoh et al. 2003; Hyder et al. 2006; Magistretti 2006). The brain can use fuels other than glucose from the circulation if their circulating levels rise high enough to enter the brain in quantity. A commonly cited example is ketone bodies that are elevated during prolonged fasting (Owen et al.
2003; Hyder et al. 2006; Magistretti 2006). The brain can use fuels other than glucose from the circulation if their circulating levels rise high enough to enter the brain in quantity. A commonly cited example is ketone bodies that are elevated during prolonged fasting (Owen et al. 1969) and during breast feeding in infants (Nehlig 2004). Another example is lactate that is sufficiently elevated during very vigorous exercise (Dalsgaard 2006). Nonetheless, among the potential substrates that normally circulate, including β-hydroxybutyrate and lactate, only injection of glucose has been found to rescue the brain of a hypoglycemic animal (Clarke and Sokoloff 1994; Won et al.