Impaired glucose tolerance and diabetes in obesity: A 6-year follow-up study of glucose metabolism

Jallut, D; Golay, Alain; Munger, R.; Frascarolo, Philippe; Schütz, Y.; Jéquier, E; Felber, J. P.

doi:10.1016/0026-0495(90)90168-c

Cited by 73 publications

(56 citation statements)

References 27 publications

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“…39 It showed evolution of obesity toward diabetes through the rise in glycemia and impairment of nonoxidative glucose disposal during a 3 h OGTT (Figure 6). In the course of the 6 y of observations, some of the obese glucose tolerant patients became diabetic.…”

Section: Studies On Obesity Durationmentioning

confidence: 99%

“…Evolution of glucose storage measured as nonoxidative glucose disposal and D glucose (increment over basal levels) during a 100 g oral glucose tolerance test between the first and the second test in a 6 y follow-up of obese subjects presenting with normal glucose tolerance, impaired glucose tolerance, and hyperinsulinemic diabetes (from Jallut et al 39 ).…”

Section: Figurementioning

confidence: 99%

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Pathways from obesity to diabetes

2002

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The relationship between obesity and type 2 diabetes has been known for decades and the recent important increase in such diseases represents a major medical problem worldwide. Several prospective studies present both impaired insulin release and insulin resistance as the major factors for the development of type 2 diabetes. The factor that dominates in obesity is the permanent elevation of plasma FFA and the predominant utilization of lipids by the muscle inducing a diminution of glucose uptake and, therefore, insulin resistance. The rise in insulin secretion appears to be a compensatory mechanism that responds to the increased levels of circulating glucose. The fall in insulin secretion occurs as a late phenomenon. The present review aims at analysing the mechanisms that lead human obesity to type 2 diabetes and using the pathophysiological information for the prevention of diabetes. The partial reversibility of the evolution of obesity towards diabetes is well demonstrated today by lifestyle changes and multidisciplinary weight loss programs.

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Section: Studies On Obesity Durationmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Pathways from obesity to diabetes

2002

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“…Obesity and type II diabetes mellitus (T2DM) are currently two pan-endemic health problems in both developed and developing countries and is associated with considerable increase in morbidity and mortality [1][2][3][4][5]. Obesity is associated with increased mortality, especially when it coexists with diabetes [4].…”

Section: Introductionmentioning

confidence: 99%

Improvement of Insulin Resistance After Obesity Surgery: A Comparison of Gastric Banding and Bypass Procedures

Lee

Lee²,

Ser

et al. 2008

OBES SURG

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“…In man, cross-sectional studies suggested the existence of a progressive evolution of the obese subjects to hyperinsulin- aemia, subsequent glucose intolerance and diabetes due to pancreatic decompensation. Such studies failed, however, to pin-point any initial cause(s) in such series of events [1,2].Investigation carried out in animal models potentially allows for an understanding of the aetiology of obesity syndromes. In this respect, it is noteworthy that chronic intracerebroventricular (i.c.v.)…”

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confidence: 99%

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confidence: 99%

Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats

et al. 1994

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Summary Intracerebroventricular neuropeptide Y (NPY) administration to normal rats for 7 days produced a sustained, threefold increase in food intake, resulting in a body weight gain of more than 40 g. Basal plasma insulin and triglyceride levels were increased in NPY-treated compared to vehicle-infused rats by about four-and two-fold, respectively. The glucose utilization index of white adipose tissue, measured by the labelled 2-deoxy-D-glucose technique was four times higher in NPY-treated rats compared to controls. This change was accompanied by an increase in the insulin responsive glucose transporter protein (GLUT 4). In marked contrast, muscle glucose utilization was decreased in NPY-treated compared to vehicle-infused animals. This change was accompanied by an increase in triglyceride content. When NPY-treated rats were prevented from overeating, there was no decrease in muscle glucose uptake, nor was there an increase in muscle triglyceride content. This suggests that muscle insulin resistance of ad libitum-fed NPY-treated rats is due to a glucose-fatty acid (Randle) cycle. When intracerebroventricular NPY administration was stopped and rats kept without any treatment for 7 additional days, all the abnormalities brought about by the neuropeptide were normalized. A tonic central effect of NPY is therefore needed to elicit and maintain most of the hormonal and metabolic abnormalities observed in the present study. Such abnormalities are analogous to those seen in the dynamic phase of obesity syndromes in which high hypothalamic NPY levels have been reported. [Diabetologia (1994[Diabetologia ( ) 37: 1202[Diabetologia ( -1208 Key words Intracerebroventricular (i.c.v.), neuropeptide Y (NPY), food intake, body weight gain, in vivo glucose uptake, muscle insulin resistance.Obesity is a pathological condition characterized by an imbalance between caloric intake and total energy expenditure. Hyperinsulinaemia and insulin resistance are the most prominent facets of this syndrome. The initial cause(s) that ultimately lead to obesity are yet to be determined. In man, cross-sectional studies suggested the existence of a progressive evolution of the obese subjects to hyperinsulin- aemia, subsequent glucose intolerance and diabetes due to pancreatic decompensation. Such studies failed, however, to pin-point any initial cause(s) in such series of events [1,2].Investigation carried out in animal models potentially allows for an understanding of the aetiology of obesity syndromes. In this respect, it is noteworthy that chronic intracerebroventricular (i.c.v.) neuropeptide Y (NPY) administration to normal rats produced several of the behavioral, hormonal, and metabolic changes observed in the dynamic phase of the genetic or hypothalamic obesity syndromes [3][4][5][6][7][8]. Thus, as in young genetically obese animals, chronic i. c. v. NPY administration to normal rats for 7 days resulted in increased food intake, body weight, liver and adipose tissue lipogenic activity, together with a state of muscle insulin resistance [9...

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Impaired glucose tolerance and diabetes in obesity: A 6-year follow-up study of glucose metabolism

Cited by 73 publications

References 27 publications

Pathways from obesity to diabetes

Pathways from obesity to diabetes

Improvement of Insulin Resistance After Obesity Surgery: A Comparison of Gastric Banding and Bypass Procedures

Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats

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