scholarly journals PPARαAgonist Fenofibrate Reduced the Secreting Load ofβ-Cells in Hypertriglyceridemia Patients with Normal Glucose Tolerance

PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-7
Author(s):  
Jia Liu ◽  
Rui Lu ◽  
Ying Wang ◽  
Yanjin Hu ◽  
Yumei Jia ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Density Lipoprotein ◽  
Normal Glucose Tolerance ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Cell Dysfunction ◽  
Fenofibrate Treatment ◽  
Normal Glucose

Hypertriglyceridemia is an important risk factor associated with insulin resistance andβ-cell dysfunction. This study investigated the effects of hypertriglyceridemia and fenofibrate treatment on insulin sensitivity andβ-cell function in subjects with normal glucose tolerance. A total of 1974 subjects with normal glucose tolerance were divided into the normal TG group (NTG group,n=1302) and hypertriglyceridemia group (HTG group,n=672). Next, 92 patients selected randomly from 672 patients with hypertriglyceridemia were assigned to a 24-week fenofibrate treatment. The HTG group had increased waist circumference (WC), body mass index (BMI), homeostasis model assessment of insulin resistance (HOMA-IR), and homeostasis model assessment ofβ-cell function (HOMA-β) and decreased high-density lipoprotein cholesterol (HDL-C) compared with the NTG group (allP<0.01). The 24-week fenofibrate treatment significantly decreased the WC, BMI, TG, HOMA-IR, and HOMA-βlevels and increased the HDL-C levels in the patients with hypertriglyceridemia (WC, BMI, and HOMA-IR:P<0.05; TG, HDL-C, and HOMA-β:P<0.01). The fenofibrate treatment significantly alleviated insulin resistance and reduced the secreting load ofβ-cells in the hypertriglyceridemia patients with normal glucose tolerance.

scholarly journals Insulin Resistance and Beta Cell Dysfunction in Severe Falciparum Malaria with Multi Organ Dysfunction Syndrome (MODS)

2020 ◽  
Vol 5 (8) ◽  
pp. 1756-1759
Author(s):  
Manoj Kumar Mohapatra ◽  
Muralidhar Anantrao Sangle ◽  
Prafulla Kumar Bariha
Keyword(s):  
Insulin Resistance ◽  
Falciparum Malaria ◽  
Organ Dysfunction ◽  
Cell Function ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Β Cell Function ◽  
Severe Falciparum Malaria

Insulin Resistance is a major factor among patients with critical illness due to various causes. Severe falciparum malaria with MODS diagnosed as per the criteria of MSS and admitted to the Medical ward of our hospital were assessed for IR and β cell function by using homeostasis model assessment. 75 consecutive patients of SFM admitted to the Medical ward of our hospital were included in this study. Malaria was diagnosed as per criteria of WHO and organ dysfunction was diagnosed as per Malaria Severity Score. Insulin Resistance and β cell function was assessed by using homeostasis model assessment on Day-1 and Day-7. Out of 75 patients of severe falciparum malaria with MODS 2, 3, 4, and 5 organ dysfunctions constituted 16 (21.3%), 34 (45.3%), 16 (21.3%), and 9 (12.0%) patients, respectively.Hepatic failure was the most common organ system failure (n=58; 77.3%), followed by neurological (n=50;66.6%) ,renal (n=40;53.3%), hematological (n=30; 40.0%), and, respiratory failure ( n=15; 20.0%). Hyperglycemia was present in 25 (33.3%) cases where as normoglycemia was present in 50 (66.6%) cases. The values of FBS, Tg, insulin, IR, and β cell function decreased on Day-7 compared to Day-1 after recovery from critically ill state. The patients who died had a high insulin value, IR, but low β cell dysfunction compared to the survivors. This study showed that IR and β cell dysfunction were associated with severe malaria with MODS with increased mortality.

scholarly journals The Normal Glucose Tolerance Continuum in Obese Youth: Evidence for Impairment in β-Cell Function Independent of Insulin Resistance

2005 ◽  
Vol 90 (2) ◽  
pp. 747-754 ◽  
Author(s):  
Catherine W. Yeckel ◽  
Sara E. Taksali ◽  
James Dziura ◽  
Ram Weiss ◽  
Tania S. Burgert ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Glucose Tolerance ◽  
Β Cell ◽  
Obese Youth ◽  
Normal Glucose ◽  
Β Cell Function

scholarly journals The Comparison of Glycated Hemoglobin and Homeostasis Model Assessment Values to 30, 60 and 90-Min Glucose Levels During OGTT in Subjects with Normal Glucose Tolerance

2014 ◽  
Vol 33 (3) ◽  
pp. 237-244
Author(s):  
Şerif Ercan ◽  
Nihal Yücel ◽  
Asuman Orçun
Keyword(s):  
Glucose Tolerance ◽  
Glycated Hemoglobin ◽  
Normal Glucose Tolerance ◽  
Oral Glucose ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Glucose Levels ◽  
Increased Risk ◽  
Normal Glucose ◽  
Optimal Values

Abstract Background: The subjects with impaired glucose tolerance have an increased risk for future type 2 diabetes (T2DM); however, a significant number of individuals who develop T2DM have normal glucose tolerance (NGT) at baseline. The study aims to compare glycated hemoglobin (HbA1C) and homeostasis model assessment (HOMA-IR) levels to 30, 60 and 90-min glucose levels in subjects with NGT. Methods: A 75-g oral glucose tolerance test (OGTT) at 0, 30, 60, 90 and 120-min was performed in 1118 subjects without known T2DM. Blood samples were also drawn for fasting insulin and HbA1C levels. Results: Forty percent of the subjects with NGT had increased post-challenge values above the determined optimal glucose levels (10.2, 10.3 and 8.9 mmol/L at 30, 60 and 90-min, respectively). Compared to the subjects with NGT whose glucose levels were below the determined optimal values at 30, 60 and 90-min, we found significantly elevated HbA1C and HOMA-IR levels in the subjects with NGT whose glucose levels were above the determined optimal values (p<0.001). Conclusions: We conclude that the subjects with NGT have different HbA1C and HOMA-IR levels considering glucose levels measured earlier than at 2-h during OGTT. Further well-designed prospective studies are needed to define the significance of 30-min, 60-min and 90-min glucose levels in the prediction of disease in subjects with T2DM.

scholarly journals Serum apoA1 (Apolipoprotein A-1), Insulin Resistance, and the Risk of Gestational Diabetes Mellitus in Human Pregnancy—Brief Report

2019 ◽  
Vol 39 (10) ◽  
pp. 2192-2197 ◽  
Author(s):  
Ravi Retnakaran ◽  
Chang Ye ◽  
Philip W. Connelly ◽  
Anthony J. Hanley ◽  
Mathew Sermer ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Density Lipoprotein ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Model Assessment ◽  
Human Pregnancy ◽  
Matsuda Index ◽  
Β Cell Function

Objective: apoA1 (apolipoprotein A-1) is the main lipoprotein associated with HDL (high-density lipoprotein) cholesterol. It was recently reported that intravenous infusion of apoA1 could lower insulin resistance in pregnant rats, leading to the suggestion that apoA1 could provide a target for reducing pregnancy-induced insulin resistance and the risk of gestational diabetes mellitus (GDM) in humans. However, the effects of apoA1 on insulin resistance and risk of GDM in human pregnancy are not known. Thus, we sought to systematically evaluate the relationships of apoA1 with glucose homeostasis and metabolic function in pregnant women. Approach and Results: In this study, 870 pregnant women were recruited in late second trimester and underwent metabolic characterization, including an oral glucose tolerance test on which 214 were diagnosed with GDM. Metabolic characterization included assessment of glucose tolerance, insulin sensitivity/resistance (Matsuda index, homeostasis model assessment of insulin resistance), pancreatic β-cell function, lipids (LDL [low-density lipoprotein] cholesterol, HDL cholesterol, triglycerides, apoB [apolipoprotein B], and apoA1), CRP (C-reactive protein), and adiponectin. Serum apoA1 was strongly correlated with HDL (r=0.79, P <0.0001) and weakly so with adiponectin (r=0.12, P =0.0004) but showed no association with measures of insulin sensitivity/resistance, β-cell function, glycemia, or CRP. There were no significant differences across apoA1 tertiles in mean adjusted Matsuda index ( P =0.24), homeostasis model assessment of insulin resistance ( P =0.08), or area under the glucose curve on the oral glucose tolerance test ( P =0.96). Moreover, there were no differences in risk of GDM across tertiles of apoA1, both before ( P =0.67) and after covariate adjustment ( P =0.78). Conclusions: Serum apoA1 is not associated with insulin resistance or the risk of GDM in human pregnancy.

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