Incidence of Type II Diabetes in Mexican Americans Predicted by Fasting Insulin and Glucose Levels, Obesity, and Body-Fat Distribution

Haffner, Steven M.; Stern, Michael P.; Mitchell, Braxton D.; Hazuda, Helen P.; Patterson, Judith K.

doi:10.2337/diab.39.3.283

Cited by 297 publications

(163 citation statements)

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“…Like the Pima Indians [3], Mexican Americans are very insulin-resistant and have a high incidence of Type 2 diabetes (T2DM) [4,5]. The goal of the SAM study was to relate the severity of glucose intolerance to the severity of beta-cell dysfunction and insulin resistance in muscle and the liver.…”

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confidence: 99%

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

et al. 2004

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“…Cross-sectional [3,4,5] and prospective [6,7,8] studies have shown an association between age and body mass index and the prevalence and incidence of Type 2 diabetes. These associations have been consistently reported from different ethnic groups.…”

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Age, body mass index and Type 2 diabetes?associations modified by ethnicity

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2003

Diabetologia

175

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Aims/hypothesis. The aim of this study was to assess the effect of ethnicity on the association between age and body mass index as well as the prevalence of diabetes. Methods. We selected population-based studies carried out after 1980 in the DECODE/A studies representing different ethnic groups: 11 European, 1 Maltese, 3 Indian, 2 Chinese and 3 Japanese surveys. The total numbers of subjects were 14,240 men and 15,129 women who were 30 to 89 years of age. Diabetes was diagnosed according to the 1999 World Health Organization criteria based on a standard 75 g OGTT. Sexspecific prevalence of diabetes by age and BMI was stratified by ethnic group, in particular the interaction of ethnicity on the associations between age/BMI and the prevalence of diabetes.Results. The prevalence of diabetes was higher in studies from India and Malta compared to Japan, China, and the rest of Europe. The association between BMI and diabetes, adjusted for age, showed noticeable differences between the ethnic groups with an increase in prevalence starting at a BMI between 15 and 20 kg/m 2 in the Maltese and Indian populations compared to 25 kg/m 2 in Europeans. Conclusion/interpretation. The effect of BMI on the age-adjusted prevalence of Type 2 diabetes was modified by ethnicity with considerably lower thresholds in Indian and Maltese subjects compared to those from the rest of Europe. This difference should be reflected in national and international recommendations regarding "optimal" BMI.

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“…Both insulin resistance [2] and deficient insulin secretion [3] have been postulated as antecedents of NIDDM. Prospective studies are useful in elucidating the complex relationship between abnormal insulin secretion and peripheral insulin resistance in the pathogenesis of NIDDM.Previous prospective studies have shown that hyperinsulinaemia is a strong predictor of NIDDM [4][5][6][7][8][9][10][11]. Insulin resistance has been inferred on the basis of hyperinsulinaemia in these studies of prediabetic subjects; in non-diabetic subjects, there is a Diabetologia (1997) Summary Although insulin resistance and decreased insulin secretion are characteristic of established non-insulin-dependent diabetes mellitus (NIDDM), which of these metabolic abnormalities is the primary determinant of NIDDM is still controversial.…”

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Total immunoreactive proinsulin, immunoreactive insulin and specific insulin in relation to conversion to NIDDM: the Mexico City Diabetes Study

et al. 1997

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Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by peripheral insulin resistance, beta-cell failure, and increased hepatic glucose production [1]. In diabetic subjects, these metabolic abnormalities interact in a complex fashion to cause and sustain hyperglycaemia. However, there continues to be controversy about which of these abnormalities is primary. Both insulin resistance [2] and deficient insulin secretion [3] have been postulated as antecedents of NIDDM. Prospective studies are useful in elucidating the complex relationship between abnormal insulin secretion and peripheral insulin resistance in the pathogenesis of NIDDM.Previous prospective studies have shown that hyperinsulinaemia is a strong predictor of NIDDM [4][5][6][7][8][9][10][11]. Insulin resistance has been inferred on the basis of hyperinsulinaemia in these studies of prediabetic subjects; in non-diabetic subjects, there is a Diabetologia (1997) Summary Although insulin resistance and decreased insulin secretion are characteristic of established non-insulin-dependent diabetes mellitus (NIDDM), which of these metabolic abnormalities is the primary determinant of NIDDM is still controversial. A disproportionate increase in the proinsulin to insulin ratio has been proposed as a marker of compromised insulin secretion. We examined the association of fasting immunoreactive insulin (which cross-reacts with proinsulin), specific insulin (which does not cross-react with proinsulin), total immunoreactive proinsulin (or insulin precursors), and the fasting proinsulin/specific insulin ratio to the risk of developing NIDDM in the 3.25-year follow-up of the Mexico City Diabetes Study. These measurements were made in 85 subjects who subsequently converted to NIDDM (prediabetic subjects) and in 85 age and gender matched subjects who remained non-diabetic at follow-up (control subjects). Immunoreactive insulin, proinsulin and the proinsulin/specific insulin ratio were significantly higher in prediabetic than in control subjects. However, the relation between specific insulin and the development of NIDDM was weaker than for proinsulin or immunoreactive insulin. After further adjustment for obesity, body fat distribution and glucose tolerance status, proinsulin and the proinsulin/specific insulin ratio, but not specific or immunoreactive insulin, predicted conversion to NIDDM. A high proinsulin/specific insulin ratio predicted conversion to NIDDM both in subjects with normal and those with impaired glucose tolerance at baseline. We conclude that in prediabetic subjects increased proinsulin, a marker of islet cell distress or compromised insulin secretion, is associated with rapid conversion (within 3.25 years) to NIDDM even in obese populations. [Diabetologia (1997) 40: 830-837]

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Incidence of Type II Diabetes in Mexican Americans Predicted by Fasting Insulin and Glucose Levels, Obesity, and Body-Fat Distribution

Cited by 297 publications

References 0 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

Age, body mass index and Type 2 diabetes?associations modified by ethnicity

Total immunoreactive proinsulin, immunoreactive insulin and specific insulin in relation to conversion to NIDDM: the Mexico City Diabetes Study

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