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Glucose Homeostasis and Diabetes
Abstract
Glucose is a hexose sugar vital as a substrate for energy metabolism. Glucose represents an essential energy substrate for many tissues and in the brain, it is an obligatory energy source.It is found in its monosaccharide form in some citrus fruits, and in the disaccharides maltose, lactose and sucrose, and in the polysaccharide starch. Within the body glucose is stored as glycogen; occasionally, other compounds may be modified to create glucose e.g. in starvation.Glucose is under the regulation of a homeostatic control system which aims to keep the fasting plasma concentration within narrow limits. Insulin-dependent diabetics are prone to fluctuations out of range: hyperglycaemia and hypoglycaemia following treatment.
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Patients with sepsis, burn, or trauma commonly enter a hypermetabolic stress state that is associated with a number of alterations in carbohydrate metabolism. These alterations include enhanced peripheral glucose uptake and utilization, hyperlactatemia, increased glucose production, depressed glycogenesis, glucose intolerance, and insulin resistance. The hypermetabolic state is induced by the area of infection or injury as well as by organs involved in the immunologic response to stress; it generates a glycemic milieu that is directed toward satisfying an obligatory requirement for glucose as an energy substrate. This article reviews experimental and clinical data that indicate potential mechanisms for these alterations and emphasizes aspects that have relevance for the clinician.
The past 20 years have witnessed a remarkable increase in our knowledge of the cellular and molecular mechanisms that underlie the diverse actions of insulin, the central hormone of metabolic regulation. Interest in the molecular details of insulin action has been heightened by the prevalence of insulin resistance and by the fact that insulin resistance has a key role in the pathogenesis of many disorders, including obesity, diabetes mellitus, ovarian hyperan-drogenism, and possibly hypertension. In this review, we discuss current concepts of the mechanisms of insulin action and insulin resistance and the implications of insulin resistance for a variety of . . .
Type II diabetes remains a genetic nightmare. The major problem is identifying suitable pedigrees, sib-pairs, and populations for study. Segregation analysis data suggest that type II diabetes is likely to be polygenic, although one or more major genes could also be involved. This and the high prevalence of diabetes affect the strategies for searching for genetic mutations. Linkage analysis in classical type II diabetes pedigrees is unlikely to be successful. In addition, affected sib-pair analysis is limited because both parents are often affected, leading to bilineal inheritance. Sib-pairs with both parents alive are unusual, so identity by descent analysis is rarely feasible. Strategies to reduce bilineal inheritance by identifying sib-pairs with one known nondiabetic parent or with the second sibling having mild subclinical diabetes may be worthwhile. Identification of individuals or pedigrees with an unusual phenotype that suggests a single gene disorder, such as maturity-onset diabetes of the young, will continue to be important, for this allows linkage analysis with markers near candidate genes and exclusion mapping of chromosomal regions using highly polymorphic markers. Population association studies with candidate genes can detect mutations that have a minor role in the majority proportion of diabetic subjects, but large numbers are required and great care must be taken to exclude ethnic group differences between the diabetic and normoglycemic populations. The study of small inbred communities might be helpful because they may have fewer diabetogenic genes than outbred populations, and this would increase the power of sib-pair and population association studies. Direct screening for mutations in candidate genes (with single-strand conformation polymorphism or heteroduplex screening or with direct sequencing) in patients with the appropriate pathophysiological abnormality can be a successful strategy. The identification of well-defined diabetic pedigrees, sib-pairs, and suitable matched diabetic and nondiabetic populations will be key to the discovery of the genes for diabetes.
- F M Ashcroft
- S J H Ashcroft
Ashcroft F.M., Ashcroft S.J.H., (1992), Insulin. Molecular biology to pathology;1-418.