Relationship of insulin clearance and secretion to insulin sensitivity in non‐diabetic Mexican Americans

Haffner, Steven M.; Stern, Michael P.; Watanabe, Richard M.; Bergman, Richard N.

doi:10.1111/j.1365-2362.1992.tb01819.x

Cited by 57 publications

(39 citation statements)

References 42 publications

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“…Differences in insulin sensitivity and ␤-cell function between non-Hispanic whites and various Latino subgroups remain to be determined. Our findings suggest that data obtained from previous studies may not be applicable to other Latinos as a group, particularly the findings that Latinos of Mexican (San Antonio, TX) and Spanish (San Luis Valley, CO) origin are less insulin sensitive than non-Hispanic whites (31,32). These findings may have been inappropriately extrapolated to other non-MexicanAmerican Latino subgroups, as studies in other Latino subgroups are limited.…”

Section: ␤-Cell Functioncontrasting

confidence: 37%

Ethnic Differences in Insulin Sensitivity and β-Cell Function in Premenopausal or Early Perimenopausal Women Without Diabetes

Torréns¹,

et al. 2004

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OBJECTIVE -To assess differences in insulin sensitivity and ␤-cell function between nondiabetic premenopausal or early perimenopausal non-Hispanic white women and African American, Chinese American, Japanese American, and non-Mexican-American Latino women. RESEARCH DESIGN AND METHODS -Homeostasis model assessments (HOMAs)of insulin sensitivity (HOMA%S) and ␤-cell function (HOMA%␤) were used. Stepwise multivariable ethnic-specific ANCOVA models were used to compare HOMA%S and HOMA%␤ between non-Hispanic whites and each of the four ethnic groups.RESULTS -HOMA%S was lower in African Americans, Chinese Americans, and Japanese Americans when compared with non-Hispanic white women after correcting for waist circumference, presence of impaired fasting glucose, and site. Significant differences persisted only between African Americans and non-Hispanic whites after inclusion of triglycerides in the model. Triglycerides indirectly corrected for the differences in HOMA%S in the other two groups. There were no differences in HOMA%S between the non-Mexican-American Latinos and the non-Hispanic whites. Japanese Americans and Chinese Americans had lower HOMA%␤ than non-Hispanic whites, whereas African Americans had higher HOMA%␤ than non-Hispanic whites after correcting for confounders. HOMA%␤ was similar between non-Mexican-American Latinos and non-Hispanic whites.CONCLUSIONS -These data suggest that type 2 diabetes prevention strategies for AfricanAmerican women should initially target decreased insulin sensitivity, whereas strategies for Japanese-American and Chinese-American women may initially need to target both decreased insulin sensitivity and ␤-cell function.

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Section: ␤-Cell Functioncontrasting

confidence: 37%

Ethnic Differences in Insulin Sensitivity and β-Cell Function in Premenopausal or Early Perimenopausal Women Without Diabetes

Torréns¹,

et al. 2004

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“…Our observations lead us to propose a second complimentary mechanism whereby peripheral insulin levels are maintained through a decrease in hepatic insulin clearance. The C-peptide:insulin ratio is an index of hepatic insulin clearance [31][32][33], and was found to be markedly decreased in the relatives (Table 2). Haffner and colleagues reported decreased hepatic insulin clearance in non-diabetic Mexican Americans when compared with non-Hispanic white control subjects [33], and proposed that it represented an adaptive response to maintain adequate circulating insulin levels in the presence of insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Multiple metabolic abnormalities in normal glucose tolerant relatives of NIDDM families

et al. 1997

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Non-insulin-dependent diabetes mellitus (NIDDM) is a complex metabolic condition characterised by both impaired insulin secretion and insulin resistance [1]. It is also recognised that elevated circulating proinsulin levels are an important and consistent feature of NIDDM [2][3][4][5], and may represent a specific defect of pancreatic beta-cell function. There is continuing debate as to whether insulin deficiency or insulin resistance represents the primary abnormality which predisposes to the development of NIDDM [6], although it is clear that comparative insulin deficiency is a sine qua non for NIDDM to develop [7].In an attempt to identify the early fundamental abnormalities, non-diabetic first degree relatives of NIDDM patients have been studied, as they have a 40 % lifetime risk of progressing to diabetes [8]. However, such an approach has so far failed to clarify matters, as some studies have found a principal defect of insulin secretion [9-13], several have suggested that Diabetologia (1997Diabetologia ( ) 40: 1185Diabetologia ( -1190 Multiple metabolic abnormalities in normal glucose tolerant relatives of NIDDM families Summary Non-diabetic first degree relatives of noninsulin-dependent diabetic (NIDDM) families are at increased risk of developing diabetes mellitus, and have been studied to identify early metabolic abnormalities. Hormone concentrations measured by specific enzyme immunoassays were assessed in non-diabetic relatives of North European extraction, and control subjects with no family history of diabetes were matched for age, sex and ethnicity. A 75-g oral glucose tolerance test was conducted and those with newly diagnosed NIDDM were excluded. Basal insulin resistance was determined by homeostasis model assessment (HOMA), and hepatic insulin clearance by C-peptide:insulin molar ratio. Relatives (n = 150) were heavier (BMI: p < 0.0001) than the control subjects (n = 152), and had an increased prevalence of impaired glucose tolerance (15 vs 3 %, p < 0.01). The relatives had increased fasting proinsulin levels and decreased C-peptide levels following the glucose load, while insulin levels were increased at all time points. To examine whether the differences in hormone levels were secondary to the differences in glucose tolerance and adiposity, we studied 100 normal glucose tolerant relatives and control subjects pairmatched for age, sex, waist-hip ratio and BMI. The differences in proinsulin levels were no longer apparent. However, the relatives remained more insulin resistant, and had decreased C-peptide levels and Cpeptide:insulin ratios at all time points. In conclusion, we have identified several metabolic abnormalities in the normal glucose tolerant relatives, and propose that the decreased hepatic insulin clearance helps to maintain normoglycaemia in the face of combined insulin resistance and decreased insulin secretion. [Diabetologie (1997[Diabetologie ( ) 40: 1185[Diabetologie ( -1190

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“…[23][24][25][26][27] It has been suggested that decreased insulin clearance compensates for decreased insulin sensitivity or vice versa. [23][24][25][26][27][28] However, experimental models suggest that the mechanisms of insulin clearance and action may be physiologically linked. In hepatocytes, the binding of insulin to its receptor is the first step for initiation of intracellular insulin signaling cascade and for endocytosis and degradation of insulin by insulin-degrading enzyme.…”

Section: Discussionmentioning

confidence: 99%

Impaired Glucose and Insulin Homeostasis in Moderate-Severe CKD

Zelnick

Afkarian

Ayers

et al. 2016

JASN

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Kidney disease leads to clinically relevant disturbances in glucose and insulin homeostasis, but the pathophysiology in moderate-severe CKD remains incompletely defined. In a cross-sectional study of 59 participants with nondiabetic CKD (mean eGFR =37.6 ml/min per 1.73 m 2 ) and 39 healthy control subjects, we quantified insulin sensitivity, clearance, and secretion and glucose tolerance using hyperinsulinemiceuglycemic clamp and intravenous and oral glucose tolerance tests. Participants with CKD had lower insulin sensitivity than participants without CKD (mean[SD] 3.9[2.0] versus 5.0 [2.0] mg/min per mU/ml; P,0.01). Insulin clearance correlated with insulin sensitivity (r=0.72; P,0.001) and was also lower in participants with CKD than controls (876 [226] versus 998 [212] ml/min; P,0.01). Adjustment for physical activity, diet, fat mass, and fatfree mass in addition to demographics and smoking partially attenuated associations of CKD with insulin sensitivity (adjusted difference, 20.7; 95% confidence interval, 21.4 to 0.0 mg/min per mU/ml) and insulin clearance (adjusted difference, 285; 95% confidence interval, 2160 to 210 ml/min). Among participants with CKD, eGFR did not significantly correlate with insulin sensitivity or clearance. Insulin secretion and glucose tolerance did not differ significantly between groups, but 65% of participants with CKD had impaired glucose tolerance. In conclusion, moderate-severe CKD associated with reductions in insulin sensitivity and clearance that are explained, in part, by differences in lifestyle and body composition. We did not observe a CKD-specific deficit in insulin secretion, but the combination of insulin resistance and inadequate augmentation of insulin secretion led to a high prevalence of impaired glucose tolerance.

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Relationship of insulin clearance and secretion to insulin sensitivity in non‐diabetic Mexican Americans

Cited by 57 publications

References 42 publications

Ethnic Differences in Insulin Sensitivity and β-Cell Function in Premenopausal or Early Perimenopausal Women Without Diabetes

Ethnic Differences in Insulin Sensitivity and β-Cell Function in Premenopausal or Early Perimenopausal Women Without Diabetes

Multiple metabolic abnormalities in normal glucose tolerant relatives of NIDDM families

Impaired Glucose and Insulin Homeostasis in Moderate-Severe CKD

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