scholarly journals Genetic Variants Related to Cardiometabolic Traits Are Associated to B Cell Function, Insulin Resistance, and Diabetes Among AmeriCan Indians: The Strong Heart Family Study

2018 ◽  
Vol 9 ◽  
Author(s):  
Poojitha Balakrishnan ◽  
Dhananjay Vaidya ◽  
V. Saroja Voruganti ◽  
Karin Haack ◽  
Jack W. Kent ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
B Cell ◽  
American Indians ◽  
Genetic Variants ◽  
Cell Function ◽  
Family Study ◽  
B Cell Function ◽  
Cardiometabolic Traits ◽  
Strong Heart Family Study

Dexamethasone-induced insulin resistance enhances B cell responsiveness to glucose level in normal men

1984 ◽  
Vol 247 (5) ◽  
pp. E592-E596 ◽  
Author(s):  
J. C. Beard ◽  
J. B. Halter ◽  
J. D. Best ◽  
M. A. Pfeifer ◽  
D. Porte
Keyword(s):  
Insulin Resistance ◽  
B Cell ◽  
Glucose Level ◽  
Cell Function ◽  
Insulin Level ◽  
Glucose Levels ◽  
B Cell Function ◽  
Normal Men ◽  
Insulin Responses ◽  
Effect Of Glucose

To determine whether islet adaptation during insulin resistance involves increased responsiveness to the level of plasma glucose, insulin resistance was induced in nine normal men by giving dexamethasone (Dex) (3 mg twice daily for 2 days). Plasma insulin and acute insulin responses (AIR) to isoproterenol were measured at three different glucose levels under control and Dex conditions. During Dex there were elevations above control levels of basal glucose (104 +/- 2 vs. 94 +/- 3 mg/dl) and insulin (21 +/- 3 vs. 13 +/- 2 microU/ml, both P less than 0.03). When glucose levels were raised stepwise by matching amounts using glucose clamps, AIR to isoproterenol rose as a linear function of glucose level under both conditions but rose more steeply during Dex. That is, the potentiating effect of glucose (delta AIR/delta glucose) was greater during Dex: 1.3 +/- 0.2 vs. 0.8 +/- 0.2 (P less than 0.01). Similarly, matched increments in glucose level produced greater increments in prestimulus insulin level during Dex (P less than 0.03). We conclude that 48 h of Dex raises the "gain" of the potentiating effect of glucose. Because the direct effect of glucocorticoids on B cell function has been reported to be inhibitory, the observed stimulation is likely to be a result of the insulin resistance caused by Dex.

scholarly journals Quantitative Linkage Analysis for Pancreatic B-cell Function and Insulin Resistance in a Large Twin Cohort

Diabetes ◽  
2008 ◽  
Vol 57 (4) ◽  
pp. 1120-1124 ◽  
Author(s):  
M. Falchi ◽  
S. G. Wilson ◽  
D. Paximadas ◽  
R. Swaminathan ◽  
T. D. Spector
Keyword(s):  
Insulin Resistance ◽  
Linkage Analysis ◽  
B Cell ◽  
Cell Function ◽  
Pancreatic B Cell ◽  
B Cell Function

scholarly journals Effect of nicotinic acid-induced insulin resistance on pancreatic B cell function in normal and streptozocin-treated baboons.

1991 ◽  
Vol 87 (4) ◽  
pp. 1395-1401 ◽  
Author(s):  
D K McCulloch ◽  
S E Kahn ◽  
M W Schwartz ◽  
D J Koerker ◽  
J P Palmer
Keyword(s):  
Insulin Resistance ◽  
Nicotinic Acid ◽  
B Cell ◽  
Cell Function ◽  
Pancreatic B Cell ◽  
B Cell Function

842 PREDISPOSITION TO DEVELOP DIABETES IN SUBJECTS WITH NAFLD IS RELATED TO INSULIN RESISTANCE RATHER THAN TO DECREASED B-CELL FUNCTION

2011 ◽  
Vol 54 ◽  
pp. S336-S337
Author(s):  
A. Gastaldelli ◽  
R. Petz ◽  
A. Ricotti ◽  
E. Cersosimo ◽  
K. Cusi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
B Cell ◽  
Cell Function ◽  
B Cell Function

Locus 10q24 and AS3MT Related to Arsenic Metabolism and Insulin Resistance in American Indians: the Strong Heart Family Study

2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Poojitha Balakrishnan* ◽  
Dhananjay Vaidya ◽  
Nora Franceschini ◽  
Saroja Voruganti ◽  
Matthew Gribble ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
American Indians ◽  
Family Study ◽  
Arsenic Metabolism ◽  
Strong Heart Family Study

Human aging is associated with parallel reductions in insulin and amylin release

1998 ◽  
Vol 275 (5) ◽  
pp. E785-E791 ◽  
Author(s):  
Cynthia J. Dechenes ◽  
C. Bruce Verchere ◽  
Sofianos Andrikopoulos ◽  
Steven E. Kahn
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
B Cell ◽  
Insulin Release ◽  
Cell Function ◽  
B Cell Function ◽  
Increased Risk ◽  
Older Subjects

Aging is associated with an increased risk of type 2 diabetes. To determine whether the insulin resistance of aging is associated with an increase in amylin release or whether amylin release parallels the reduction in insulin release, we studied 10 older (72 ± 2 yr) and 9 young (25 ± 1 yr) subjects. Insulin sensitivity was quantified as the insulin sensitivity index (SI) and B cell function as the acute insulin and amylin responses to iv glucose (AIRg and AARg, respectively) and iv arginine at a glucose level of >25 mM (AIRmax and AARmax). To account for the effect of SIto modulate B cell function, we calculated SI× B cell function. Older subjects were insulin resistant (SI: 4.6 ± 0.8 vs. 8.6 ± 1.4 × 10−5min−1/pM, P < 0.05). Acute responses to glucose [AIRg (older vs. young): 420 ± 106 vs. 537 ± 87 pM; AARg: 6.5 ± 1.7 vs. 9.0 ± 1.5 pM] and arginine (AIRmax: 1,096 ± 203 vs. 1,572 ± 307 pM; AARmax: 14.0 ± 3.5 vs. 16.5 ± 2.4 pM) did not differ despite the difference in SI. When adjusted for SI, insulin responses were reduced in older subjects (SI× AIRg: 1.54 ± 0.29 vs. 4.10 ± 0.63 × 10−2min−1, P = 0.001; SI× AIRmax: 4.03 ± 0.52 vs. 12.7 ± 2.9 × 10−2min−1, P < 0.01), as was amylin release (SI× AARg: 2.46 ± 0.59 vs. 6.85 ± 0.95 × 10−4min−1, P < 0.001; SI× AARmax: 4.71 ± 0.52 vs. 13.5 ± 2.2 × 10−4min−1, P < 0.001). Amylin and insulin release was proportionate, with a molar ratio of 1.5% in older and 1.4% in young subjects. Thus aging is associated with parallel impairments in the adaptation of insulin and amylin release to insulin resistance. It is unlikely that an alteration in amylin release contributes to the increased risk of type 2 diabetes.

scholarly journals Metabolic syndrome in Iraqi female patients with major β-thalassemia

2017 ◽  
Vol 27 (4) ◽  
Author(s):  
Shaemaa Hadi Abdulsada ◽  
Aliaa Hashim Farag ◽  
Hassanain Kamil ◽  
Salma Abdul-Rudha ◽  
Ali Abdulrassol Hussein
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
B Cell ◽  
Cell Function ◽  
Atherogenic Index ◽  
Control Group ◽  
Female Patients ◽  
B Cell Function ◽  
Increased Risk

Patients with β-thalassemia may have an increased risk for diabetes mellitus and cardiovascular diseases due to high level of iron which may lead to insulin resistanceand metabolic syndrome. So this study aimed to evaluate the levels of lipids profile in Iraqi female patients with β-thalassemia. Forty twofemale (age 15-30) years were enrolled in this study. Blood was collected and the sera were separated from (22) female patients with β-thalassemia who were attended the Ibn-Al-Baladi hospital from September 2012 to January 2013 and (20) healthy subject as a control group. Body mass index (BMI), lipid profile, FSG, insulin, insulin resistance, insulin sensitivity, B-cell function, iron, atherogenic index of serum were estimated.The results showed the presence of a significant increase in serum iron and significant decrease in insulin, B-cell function, LDL, VLDL, and TC in serum of patients with β-thalassemia when compared with control group. BMI also showed a significant decrease in patients when compared with the controls. Serum Insulin resistance, insulin sensitivity, HDL, TG, AIS, and FSG showed no-significant differences in patients with β-thalassemia when compared with control group. We concluded there was no metabolic syndrome in female patients with β-thalassemia.

Abstract P371: ALOX5 Haplotype, Dietary Intake of Omega-6 Fatty Acids and Obesity in American Indians: The Strong Heart Family Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Guangming Han ◽  
Shelley A Cole ◽  
Karin Haack ◽  
Ying Zhang ◽  
Barbara V Howard ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Dietary Intake ◽  
American Indians ◽  
Body Fat ◽  
Genetic Variants ◽  
Multiple Testing ◽  
Family Study ◽  
Carrier Status ◽  
Dietary Intakes ◽  
Strong Heart Family Study

Background: Obesity is a strong determinant for cardiovascular disease (CVD). It results from the complex interplay between genetic and environmental factors. Inflammation has been implicated in obesity and its related phenotypes. Leukotrienes are inflammatory mediators generated from arachidonic acid (polyunsaturated n-6 fatty acid) by the enzyme 5-lipoxygenase (5-LO). Genetic variants in genes encoding 5-LO (e.g., ALOX5) are potential contributors to obesity, probably through nutrigenetic interactions. Objectives: To examine whether genetic variants in ALOX5 are associated with obesity measures, and whether the association is modified by dietary intake of n-6 fatty acids. Methods: Thirteen tagging SNPs in ALOX5 were genotyped in 3,665 American Indians recruited by the Strong Heart Family Study from Oklahoma (OK), South/North Dakota (DK) and Arizona (AZ). Dietary intake was assessed with a food frequency questionnaire. Gene-based association and haplotype × diet interactions were investigated using generalized estimating equation, controlling for age, sex, smoking, alcohol intake, lipids, blood pressure, levels of physical activity, fibrinogen, renal function and total caloric intake. Because dietary intakes of n-3 and n-6 fatty acids are highly correlated, the nutrigenetic interactions were additionally adjusted for n-3 fatty acids. All analyses were stratified by geographic sites. Multiple testing was adjusted using the false discovery rate. Results: A 13-SNP haplotype, named HapZ, is significantly associated with obesity. Subjects carrying HapZ have significantly smaller obesity measures, including body mass index (BMI), waist circumference (WC) and body fat, compared to those not carrying this haplotype (all P<0.0001). The frequencies of HapZ among participants from OK, AZ and DK are 16.2%, 7.7% and 30.1%, respectively. Moreover, we identified a significant interaction between HapZ and dietary intake of n-6 fatty acids on obesity among participants from OK. Higher intake of n-6 fatty acids was associated with decreased level of obesity among HapZ carriers, but increased obesity level among HapZ noncarriers (Pinteraction =0.024 for BMI, Pinteraction =0.008 for WC, Pinteraction =0.003 for body fat), suggesting that the effect of n-6 fatty acids on obesity depends on the carrier status of this leukotriene haplotype. The nutrigenetic interaction was also observed in DK on BMI (Pinteraction =0.016), but not other obese parameters. Further adjustment for diabetes did not change our results. Conclusion: A novel ALOX5 haplotype is significantly and negatively associated with obesity in American Indians. Dietary intake of n-6 fatty acids modifies the apparent beneficial effect of this haplotype on obesity. If replicated, our findings could potentially lead to individualized lifestyle intervention for reducing the risk of obesity, diabetes and CVD.Funding(This research has received full or partial funding support from the American Heart Association, National Center)

Sign in / Sign up

Export Citation Format

Share Document