Effect of Serum Zinc and Copper Levels on Insulin Secretion, Insulin Resistance and Pancreatic β cell Dysfunction in US Adults: Findings from the National Health and Nutrition Examination Survey (NHANES) 2011-2012

2020 ◽  
pp. 108627
Author(s):  
Ravi Kant ◽  
Vipin Verma ◽  
Siddharth Patel ◽  
Rashmi Chandra ◽  
Rahul Chaudhary ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
National Health ◽  
Serum Zinc ◽  
Nutrition Examination Survey ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Health And Nutrition

scholarly journals Visceral Adiposity Index is associated with Insulin Resistance, impaired Insulin Secretion, and β-cell dysfunction in subjects at risk for Type 2 Diabetes

2021 ◽  
pp. 100013
Author(s):  
Froylan David Martínez-Sánchez ◽  
Valerie Paola Vargas-Abonce ◽  
Andrea Rocha-Haro ◽  
Romina Flores-Cardenas ◽  
Milagros Fernández-Barrio ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
At Risk ◽  
Insulin Secretion ◽  
Visceral Adiposity ◽  
Visceral Adiposity Index ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Impaired Insulin

Effects of pharmacological inhibition of NADPH oxidase or iNOS on pro-inflammatory cytokine, palmitic acid or H2O2-induced mouse islet or clonal pancreatic β-cell dysfunction

2010 ◽  
Vol 30 (6) ◽  
pp. 445-453 ◽  
Author(s):  
Marta Michalska ◽  
Gabriele Wolf ◽  
Reinhard Walther ◽  
Philip Newsholme
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Nadph Oxidase ◽  
Inflammatory Cytokine ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Mouse Islets ◽  
Pro Inflammatory Cytokines

Various pancreatic β-cell stressors including cytokines and saturated fatty acids are known to induce oxidative stress, which results in metabolic disturbances and a reduction in insulin secretion. However, the key mechanisms underlying dysfunction are unknown. We investigated the effects of prolonged exposure (24 h) to pro-inflammatory cytokines, H2O2 or PA (palmitic acid) on β-cell insulin secretion, ATP, the NADPH oxidase (nicotinamide adenine dinucleotide phosphate oxidase) component p47phox and iNOS (inducible nitric oxide synthase) levels using primary mouse islets or clonal rat BRIN-BD11 β-cells. Addition of a pro-inflammatory cytokine mixture [IL-1β (interleukin-1β), TNF-α (tumour necrosis factor-α) and IFN-γ (interferon-γ)] or H2O2 (at sub-lethal concentrations) inhibited chronic (24 h) levels of insulin release by at least 50% (from islets and BRIN-BD11 cells), while addition of the saturated fatty acid palmitate inhibited acute (20 min) stimulated levels of insulin release from mouse islets. H2O2 decreased ATP levels in the cell line, but elevated p47phox and iNOS levels as did cytokine addition. Similar effects were observed in mouse islets with respect to elevation of p47phox and iNOS levels. Addition of antioxidants SOD (superoxide dismutase), Cat (catalase) and NAC (N-acetylcysteine) attenuated H2O2 or the saturated fatty acid palmitate-dependent effects, but not cytokine-induced dysfunction. However, specific chemical inhibitors of NADPH oxidase and/or iNOS appear to significantly attenuate the effects of cytokines, H2O2 or fatty acids in islets. While pro-inflammatory cytokines are known to increase p47phox and iNOS levels in β-cells, we now report that H2O2 can increase levels of the latter two proteins, suggesting a key role for positive-feedback redox sensitive regulation of β-cell dysfunction.

Analysis of compensatory β-cell response in mice with combined mutations of Insr and Irs2

2007 ◽  
Vol 292 (6) ◽  
pp. E1694-E1701 ◽  
Author(s):  
Jane J. Kim ◽  
Yoshiaki Kido ◽  
Philipp E. Scherer ◽  
Morris F. White ◽  
Domenico Accili
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Cell Response ◽  
Cell Mass ◽  
Comprehensive Treatment ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Impaired Insulin

Type 2 diabetes results from impaired insulin action and β-cell dysfunction. There are at least two components to β-cell dysfunction: impaired insulin secretion and decreased β-cell mass. To analyze how these two variables contribute to the progressive deterioration of metabolic control seen in diabetes, we asked whether mice with impaired β-cell growth due to Irs2 ablation would be able to mount a compensatory response in the background of insulin resistance caused by Insr haploinsufficiency. As previously reported, ∼70% of mice with combined Insr and Irs2 mutations developed diabetes as a consequence of markedly decreased β-cell mass. In the initial phases of the disease, we observed a robust increase in circulating insulin levels, even as β-cell mass gradually declined, indicating that replication-defective β-cells compensate for insulin resistance by increasing insulin secretion. These data provide further evidence for a heterogeneous β-cell response to insulin resistance, in which compensation can be temporarily achieved by increasing function when mass is limited. The eventual failure of compensatory insulin secretion suggests that a comprehensive treatment of β-cell dysfunction in type 2 diabetes should positively affect both aspects of β-cell physiology.

Association of sodium intake with insulin resistance in Korean children and adolescents: the Korea National Health and Nutrition Examination Survey 2010

2018 ◽  
Vol 31 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Yong Min Kim ◽  
So Hyun Kim ◽  
Young Suk Shim
Keyword(s):  
Insulin Resistance ◽  
Children And Adolescents ◽  
National Health ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Nutrition Examination Survey ◽  
Creatinine Ratio ◽  
Korean Children ◽  
Urinary Creatinine ◽  
Health And Nutrition

Abstract Background: This study aimed to evaluate the relationship between sodium intake and insulin resistance indices. Methods: A total of 718 Korean children and adolescents (411 boys) aged 10–18 years who participated in the Korea National Health and Nutrition Examination Survey (KNHANES) were included in the study. The urinary sodium to urinary creatinine ratio was used as a surrogate for sodium intake. The homeostatic model assessment of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) were used as indices of insulin resistance. Results: The mean urinary sodium to urinary creatinine ratio was 11.34 in males and 10.17 in females. The urinary sodium to urinary creatinine ratio was significantly positively correlated with HOMA-IR (r=0.165, p<0.001) and inversely correlated with QUICKI (r=−0.181, p<0.001) in Pearson’s correlation analyses. In a multivariate linear regression analysis, the urinary sodium to urinary creatinine ratio was independently and significantly positively associated with HOMA-IR (β=0.073, p=0.018) and significantly inversely associated with QUICKI (β=−0.080, p=0.007) after adjustment for possible confounders. HOMA-IR was independently and significantly positively associated with the urinary sodium to urinary creatinine ratio (β=0.087, p=0.018), whereas QUICKI was independently and significantly negatively associated with the urinary sodium to urinary creatinine ratio (β=−0.097, p=0.009) after controlling for confounders. Conclusions: Our results suggest that sodium intake, as estimated by the urinary sodium to urinary creatinine ratio, may be independently associated with insulin resistance in children and adolescents.

Major Depressive Disorder and Insulin Resistance in Nondiabetic Young Adults in the United States: The National Health and Nutrition Examination Survey, 1999-2002

2010 ◽  
Vol 13 (2) ◽  
pp. 175-181 ◽  
Author(s):  
Qiuhua Shen ◽  
Sandra Bergquist-Beringer ◽  
Valmi D. Sousa
Keyword(s):  
United States ◽  
Insulin Resistance ◽  
Young Adults ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
National Health ◽  
The United States ◽  
Nutrition Examination Survey ◽  
Major Depressive ◽  
Health And Nutrition

Objective: The association between depression and insulin resistance has been evaluated in previous studies with conflicting results. This study aimed to explore the relationship between major depressive disorder (MDD) and insulin resistance among nondiabetic young adult men and women in the United States. Method: Analyses of cross-sectional data from the National Health and Nutrition Examination Survey (NHANES), 1999—2002, were conducted. The nationally representative sample consisted of 279 men and 358 women aged 20—39 years. MDD was determined by the WHO Composite International Diagnostic Interview (CIDI). Insulin resistance was measured by the homeostasis model assessment for insulin resistance. Results: Of 637 subjects, 16 men and 18 women had MDD (weighted percentage = 6.6%, SE = 1.2). Using logistic regression, no significant association was found between MDD and insulin resistance among the nondiabetic young adults in bivariate analysis (β = -0.01, OR = 0.99, 95% CI = [0.38, 2.57], p = .98). A significant interaction effect between gender and MDD was observed. For men, MDD was negatively associated with insulin resistance after adjusting for age, race/ethnicity, waist circumference, smoking status, systolic blood pressure and triglyceride level (β = -2.12, OR = 0.12, 95% CI = [0.02, 0.62], p = .01). No significant association between MDD and insulin resistance among women was found (β = 0.61, OR = 1.84, 95% CI = [0.47, 7.14], p = .38). Conclusions: Overall findings suggest there is no significant association between MDD and insulin resistance among nondiabetic young adults aged 20—39 years. However, gender differences in this relationship were noted.

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