2079-P: Racial Differences in Gut Microbiota, ß-Cell Function, Body Fat Distribution, and Their Relation with Incretins in Subjects with Normal Glucose Tolerance

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2079-P
Author(s):  
PAUL NIZIGIYIMANA ◽  
LERONG LIU ◽  
BOYA XU ◽  
TINGTING LIU ◽  
LIN GAO ◽  
...  
2019 ◽  
Author(s):  
Jing Zheng ◽  
Juan Liu ◽  
Beverly S Hong ◽  
Yanbing Li

Abstract Background: The relationship between betatrophin/ANGPTL8 and obesity has been investigated using body mass index (BMI); however, since BMI reflects overall adiposity rather than body fat distribution, it remains unclear whether fat deposition in different areas of the body affects betatrophin expression. Here, we investigated the correlation between circulating betatrophin levels and body fat distribution in patients with different glucose tolerance. Methods: In 128 participants with impaired glucose tolerance (IGT; n = 64) or normal glucose tolerance (NGT; n = 64), we measured circulating betatrophin levels by enzyme-linked immunosorbent assay and body fat distribution (subcutaneous, visceral, and limb fat) using magnetic resonance imaging (MRI) and a body fat meter. Results: After controlling for age, sex, and BMI, betatrophin was correlated positively with visceral adipose tissue-to-subcutaneous adipose tissue ratio ( VAT/SAT ratio; r = 0.339, p = 0.009) and negatively with body fat ratio (BFR; r = -0.275, p = 0.035), left lower limb fat ratio (LLR; r = -0.330, p = 0.011), and right lower limb fat ratio (RLR; r = -0.288, p = 0.027) in the NGT group, with these correlations remaining after controlling for triglycerides. VAT/SAT ratio (standardized β = 0.419, p = 0.001) was independently associated with serum betatrophin levels; however, betatrophin was not associated with body fat distribution variables in the IGT group. Conclusions: Circulating betatrophin levels correlated positively with VAT/SAT ratio and negatively with lower limb fat, but not subcutaneous or upper limb fat, in individuals with normal glucose tolerance. Thus, betatrophin may be a poten­tial biomarker for body fat distribution in individuals without glucose disorders.


2020 ◽  
Author(s):  
jing zheng(Former Corresponding Author) ◽  
Juan Liu ◽  
Beverly S Hong ◽  
Yanbing Li(New Corresponding Author)

Abstract Background: The relationship between betatrophin/ANGPTL8 and obesity has been investigated using body mass index (BMI); however, since BMI reflects overall adiposity rather than body fat distribution, it remains unclear whether fat deposition in different areas of the body affects betatrophin expression. Here, we investigated the correlation between circulating betatrophin levels and body fat distribution in patients with different glucose tolerance. Methods: We performed a cross-sectional study in 128 participants with impaired glucose tolerance (IGT; n = 64) or normal glucose tolerance (NGT; n = 64). Circulating betatrophin levels were detected by enzyme-linked immunosorbent assay. Body fat distribution (subcutaneous, visceral, and limb fat) was measured by magnetic resonance imaging (MRI) and a body fat meter.Results: After controlling for age, sex, and BMI, betatrophin was correlated positively with visceral adipose tissue-to-subcutaneous adipose tissue ratio ( VAT/SAT ratio; r = 0.339, p = 0.009) and negatively with body fat ratio (BFR; r = -0.275, p = 0.035), left lower limb fat ratio (LLR; r = -0.330, p = 0.011), and right lower limb fat ratio (RLR; r = -0.288, p = 0.027) in the NGT group, with these correlations remaining after controlling for triglycerides. VAT/SAT ratio (standardized β = 0.419, p = 0.001) was independently associated with serum betatrophin levels; however, betatrophin was not associated with body fat distribution variables in the IGT group.Conclusions: Circulating betatrophin levels correlated positively with VAT/SAT ratio and negatively with lower limb fat, but not subcutaneous or upper limb fat, in individuals with normal glucose tolerance. Thus, betatrophin may be a poten­tial biomarker for body fat distribution in individuals without glucose disorders.


2020 ◽  
Author(s):  
Jing Zheng ◽  
Juan Liu ◽  
Beverly S Hong ◽  
Weijian Ke New ◽  
Minmin Huang New ◽  
...  

Abstract Background: The relationship between betatrophin/ANGPTL8 and obesity has been investigated using body mass index (BMI); however, since BMI reflects overall adiposity rather than body fat distribution, it remains unclear whether fat deposition in different areas of the body affects betatrophin expression. Here, we investigated the correlation between circulating betatrophin levels and body fat distribution in patients with different glucose tolerance. Methods: We performed a cross-sectional study in 128 participants with impaired glucose tolerance (IGT; n = 64) or normal glucose tolerance (NGT; n = 64). Circulating betatrophin levels were detected by enzyme-linked immunosorbent assay. Body fat distribution (subcutaneous, visceral, and limb fat) was measured by magnetic resonance imaging (MRI) and a body fat meter. Results: After controlling for age, sex, and BMI, betatrophin was correlated positively with visceral adipose tissue-to-subcutaneous adipose tissue ratio ( VAT/SAT ratio; r = 0.339, p = 0.009) and negatively with body fat ratio (BFR; r = -0.275, p = 0.035), left lower limb fat ratio (LLR; r = -0.330, p = 0.011), and right lower limb fat ratio (RLR; r = -0.288, p = 0.027) in the NGT group, with these correlations remaining after controlling for triglycerides. VAT/SAT ratio (standardized β = 0.419, p = 0.001) was independently associated with serum betatrophin levels; however, betatrophin was not associated with body fat distribution variables in the IGT group. Conclusions: Circulating betatrophin levels correlated positively with VAT/SAT ratio and negatively with lower limb fat, but not subcutaneous or upper limb fat, in individuals with normal glucose tolerance. Thus, betatrophin may be a poten­tial biomarker for body fat distribution in individuals without glucose disorders.


2020 ◽  
Author(s):  
jing zheng ◽  
Juan Liu ◽  
Beverly S Hong ◽  
Yanbing Li

Abstract Background: The relationship between betatrophin/ANGPTL8 and obesity has been investigated using body mass index (BMI); however, since BMI reflects overall adiposity rather than body fat distribution, it remains unclear whether fat deposition in different areas of the body affects betatrophin expression. Here, we investigated the correlation between circulating betatrophin levels and body fat distribution in patients with different glucose tolerance.Methods: We performed a cross-sectional study in 128 participants with impaired glucose tolerance (IGT; n = 64) or normal glucose tolerance (NGT; n = 64). Circulating betatrophin levels were detected by enzyme-linked immunosorbent assay. Body fat distribution (subcutaneous, visceral, and limb fat) was measured by magnetic resonance imaging (MRI) and a body fat meter.Results: After controlling for age, sex, and BMI, betatrophin was correlated positively with visceral adipose tissue-to-subcutaneous adipose tissue ratio ( VAT/SAT ratio; r = 0.339, p = 0.009) and negatively with body fat ratio (BFR; r = -0.275, p = 0.035), left lower limb fat ratio (LLR; r = -0.330, p = 0.011), and right lower limb fat ratio (RLR; r = -0.288, p = 0.027) in the NGT group, with these correlations remaining after controlling for triglycerides. VAT/SAT ratio (standardized β = 0.419, p = 0.001) was independently associated with serum betatrophin levels; however, betatrophin was not associated with body fat distribution variables in the IGT group.Conclusions: Circulating betatrophin levels correlated positively with VAT/SAT ratio and negatively with lower limb fat, but not subcutaneous or upper limb fat, in individuals with normal glucose tolerance. Thus, betatrophin may be a poten­tial biomarker for body fat distribution in individuals without glucose disorders.


2020 ◽  
Vol 16 (7) ◽  
pp. 699-715 ◽  
Author(s):  
Georgios S. Papaetis

Background: Prediabetes is defined as a state of glucose metabolism between normal glucose tolerance and type 2 diabetes. Continuous β-cell failure and death are the reasons for the evolution from normal glucose tolerance to prediabetes and finally type 2 diabetes. Introduction: The necessity of new therapeutic approaches in order to prevent or delay the development of type 2 diabetes is obligatory. Liraglutide, a long-acting GLP-1 receptor agonist, has 97% homology for native GLP-1. Identification of the trophic and antiapoptotic properties of liraglutide in preclinical studies, together with evidence of sustained β-cell function longevity during its administration in type 2 diabetes individuals, indicated its earliest possible administration during this disease, or even before its development, so as to postpone or delay its onset. Methods: Pubmed and Google databases have been thoroughly searched and relevant studies were selected. Results: This paper explores the current evidence of liraglutide administration both in humans and animal models with prediabetes. Also, it investigates the safety profile of liraglutide treatment and its future role to postpone or delay the evolution of type 2 diabetes. Conclusion: Liralgutide remains a valuable tool in our therapeutic armamentarium for individuals who are overweight or obese and have prediabetes. Future well designed studies will give valuable information that will help clinicians to stratify individuals who will derive the most benefit from this agent, achieving targeted therapeutic strategies.


PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-7
Author(s):  
Jia Liu ◽  
Rui Lu ◽  
Ying Wang ◽  
Yanjin Hu ◽  
Yumei Jia ◽  
...  

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.


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