Sequential Changes in Serum Insulin Concentration During Development of Non-Insulin-Dependent Diabetes

Saad, MohammedF.; Pettitt, D. J.; Mott, David M.; Knowler, W. C.; Nelson, RobertG.; Bennett, P. H.

doi:10.1016/s0140-6736(89)92804-3

Cited by 261 publications

(154 citation statements)

References 39 publications

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“…A similar natural history has been shown in the Rhesus monkey [9]. This progression has been demonstrated in populations of diverse ethnic background [6,7,8,10,11,12]. In populations with a high prevalence of T2DM, insulin resistance is well established long before the development of any impairment in glucose homeostasis [1,2,3,5,6,9,10,11,12].…”

mentioning

confidence: 60%

“…It generally is accepted that the emergence of T2DM is preceded by a stage of IGT [1,2,3,6,7,8,9,10,11,12,14,16,17,18,19]. T2DM ensues when the beta cell is not able to secrete sufficient amounts of insulin to offset the severity of insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

“…According to the criteria established by the American Diabetes Association [30], IGT is defined by a 2-h plasma glucose concentration between 7.8 and 11.1 mmol/l during an OGTT. Many studies have shown that IGT individuals are resistant to the action of insulin and that the progression from IGT to T2DM is associated with a decline in beta-cell function with little additional worsening of peripheral insulin resistance [1,3,6,8,9,14,16,17,18,39]. The defect in insulin secretion in IGT individuals is most evident when the early (0-to 30-min) plasma insulin response following glucose ingestion is examined.…”

Section: Discussionmentioning

confidence: 99%

“…In the natural history of T2DM, individuals progress from normal glucose tolerance (NGT) to imThe San Antonio Metabolism (SAM) study was designed to examine the major determinants (insulin secretion and insulin sensitivity) of glucose homeostasis [1,2] in the population of South Texas, which is compaired glucose tolerance (IGT) to overt T2DM [1,2,3,6,7,8]. A similar natural history has been shown in the Rhesus monkey [9].…”

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confidence: 99%

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Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

et al. 2004

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Aims/hypothesis. Both insulin resistance and beta-cell dysfunction play a role in the transition from normal glucose tolerance (NGT) to Type 2 diabetes (T2DM) through impaired glucose tolerance (IGT). The aim of the study was to define the level of glycaemia at which beta-cell dysfunction becomes evident in the context of existing insulin resistance. Methods. Insulin response (OGTT) and insulin sensitivity (euglycaemic insulin clamp) were evaluated in 388 subjects in the San Antonio Metabolism (SAM) study (138 NGT, 49 IGT and 201 T2DM). In all subjects the insulin secretion/insulin resistance index (DeltaI/DeltaGdivided byIR) was calculated as the ratio of the increment in plasma insulin to the increment in plasma glucose during the OGTT divided by insulin resistance, as measured during the clamp. Results. In lean NGTs with a 2-h plasma glucose concentration (2-h PG) between 5.6 and 6.6 and between 6.7 and 7.7 mmol/l, there was a progressive decline in DeltaI/AGdivided byIR compared with NGTs with a 2-h PG less than 5.6 mmol/l. There was a further decline in DeltaI/DeltaGdivided byIR in IGTs with a 2-h PG between 7.8 and 9.3 and between 9.4 and 11.0 mmol/l, and in Type 2 diabetic patients with a 2-h PG greater than It. I mmol/l. Lean and obese subjects showed coincident patterns of relation of 2-h PG to DeltaI/DeltaGdivided byIR. Conclusion/interpreation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in "normal" glucose tolerant individuals

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mentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

et al. 2004

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“…Secondly, we rechecked the disease history from case records for all those with inconsistent answers on anti-hypertensive medications and excluded the patients who took drugs with BP-lowering effect for diseases other than hypertension. Subjects with IGT provide a good opportunity to study the association between hypertension and hyperinsulinaemia, since hyperinsulinaemia and insulin resistance are basic characteristics of patients with IGT, [18][19][20] and the incidence of IGT is higher in hypertensive patients. 21 In this study, the incidence of hypertension was higher in the subjects with diabetes and IGT compared to the subjects with normal glucose tolerance at follow-up.…”

Section: Discussionmentioning

confidence: 99%

Hypertension, hyperinsulinaemia and obesity in middle-aged Finns with impaired glucose tolerance

Qiao

Rajala

Keinänen‐Kiukaanniemi

1998

J Hum Hypertens

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The aim of the study was to analyse the data obtained from a 2-year follow-up study of middle-aged Finnish subjects (n = 183) with a previous history of impaired glucose tolerance (IGT) in order to elucidate the longitudinal relationships between hypertension, fasting hyperinsulinaemia and obesity. Hypertension was defined as either a systolic blood pressure (BP) of у160 mm Hg or a diastolic BP of у95 mm Hg or being on antihypertensive medication regardless of the BP value. Multiple logistic regression analysis adjusted for glucose tolerance status, serum lipids, exercise behaviour and alcohol consumption shows that the odds ratios of

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Comorbidity and Glycemic Control in Patients With Type 2 Diabetes

El‐Kebbi¹,

Ziemer²,

Cook³

et al. 2001

Arch Intern Med

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Sequential Changes in Serum Insulin Concentration During Development of Non-Insulin-Dependent Diabetes

Cited by 261 publications

References 39 publications

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study

Hypertension, hyperinsulinaemia and obesity in middle-aged Finns with impaired glucose tolerance

Comorbidity and Glycemic Control in Patients With Type 2 Diabetes

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