scholarly journals Fatty Liver Has Stronger Association With Insulin Resistance Than Visceral Fat Accumulation in Nonobese Japanese Men

2019 ◽  
Vol 3 (7) ◽  
pp. 1409-1416 ◽  
Author(s):  
Satoshi Kadowaki ◽  
Yoshifumi Tamura ◽  
Yuki Someya ◽  
Kageumi Takeno ◽  
Hideyoshi Kaga ◽  
...  

Abstract Context Asians have a high prevalence of insulin resistance, even in the nonobese state. Whereas both visceral fat accumulation (VFA) and fatty liver (FL) have been shown to be associated with insulin resistance, it is still unclear which is a better marker to predict insulin resistance in nonobese Asians. Objective The aim of this study was to investigate the relation between VFA or FL and insulin resistance in nondiabetic nonobese Japanese men who do not have diabetes. Design and Participants We studied 87 nonobese (body mass index <25 kg/m2) Japanese men without diabetes. Using a two-step hyperinsulinemic euglycemic clamp, we evaluated insulin sensitivity in adipose tissue, muscle, and liver. Intrahepatic lipid and abdominal visceral fat area were measured by 1H-magnetic resonance spectroscopy and MRI, respectively. Subjects were divided into four groups based on the presence or absence of VFA (visceral fat area ≥100 cm2) and FL (intrahepatic lipid ≥ 5%): control (non-VFA, non-FL; n = 54), VFA only (n = 18), FL only (n = 7), and VFA plus FL (n = 8). Results Subjects in the FL only and VFA plus FL groups had insulin resistance in adipose tissue and muscle, as well as relatively lower hepatic insulin sensitivity. The specific insulin sensitivities in these organs were comparable in the VFA only and control groups. Conclusions In nonobese Japanese men without diabetes, subjects with FL only or VFA plus FL but not VFA only had insulin resistance, suggesting that FL may be a more useful clinical marker than VFA to predict insulin resistance in nonobese Japanese men without diabetes.

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1854-P
Author(s):  
SATOSHI KADOWAKI ◽  
YOSHIFUMI TAMURA ◽  
YUKI SOMEYA ◽  
KAGEUMI TAKENO ◽  
TAKASHI FUNAYAMA ◽  
...  

Metabolism ◽  
2003 ◽  
Vol 52 (10) ◽  
pp. 1274-1278 ◽  
Author(s):  
Toshimitsu Yatagai ◽  
Shoichiro Nagasaka ◽  
Ataru Taniguchi ◽  
Mitsuo Fukushima ◽  
Tomoatsu Nakamura ◽  
...  

2006 ◽  
Vol 41 (5) ◽  
pp. 462-469 ◽  
Author(s):  
Yuichiro Eguchi ◽  
Takahisa Eguchi ◽  
Toshihiko Mizuta ◽  
Yasushi Ide ◽  
Tsutomu Yasutake ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0149436 ◽  
Author(s):  
Shuichiro Yamamoto ◽  
Yumi Matsushita ◽  
Toru Nakagawa ◽  
Toru Honda ◽  
Takeshi Hayashi ◽  
...  

2006 ◽  
Vol 91 (11) ◽  
pp. 4287-4294 ◽  
Author(s):  
Tania S. Burgert ◽  
Sara E. Taksali ◽  
James Dziura ◽  
T. Robin Goodman ◽  
Catherine W. Yeckel ◽  
...  

Abstract Background: Concurrent with the rise in obesity, nonalcoholic fatty liver disease is recognized as the leading cause of serum aminotransferase elevations in obese youth. Nevertheless, the complete metabolic phenotype associated with abnormalities in biomarkers of liver injury and intrahepatic fat accumulation remains to be established. Methods: In a multiethnic cohort of 392 obese adolescents, alanine aminotransferase (ALT) levels were related with parameters of insulin sensitivity, glucose, and lipid metabolism as well as adipocytokines and biomarkers of inflammation. A subset of 72 adolescents had determination of abdominal fat partitioning and intrahepatic fat accumulation using magnetic resonance imaging. Findings: Elevated ALT (&gt;35 U/liter) was found in 14% of adolescents, with a predominance of male gender and white/Hispanic race/ethnicity. After adjusting for potential confounders, rising ALT was associated with reduced insulin sensitivity and glucose tolerance as well as rising free fatty acids and triglycerides. Worsening of glucose and lipid metabolism was already evident as ALT levels rose into the upper half of the normal range (18–35 U/liter). When hepatic fat fraction was assessed using fast magnetic resonance imaging, 32% of subjects had an increased hepatic fat fraction, which was associated with decreased insulin sensitivity and adiponectin, and increased triglycerides, visceral fat, and deep to superficial sc fat ratio. The prevalence of the metabolic syndrome was significantly greater in those with fatty liver. Interpretation: Deterioration in glucose and lipid metabolism is associated even with modest ALT elevations. Hepatic fat accumulation in childhood obesity is strongly associated with the triad of insulin resistance, increased visceral fat, and hypoadiponectinemia. Hence, hepatic steatosis may be a core feature of the metabolic syndrome.


2011 ◽  
Vol 107 (10) ◽  
pp. 1429-1434 ◽  
Author(s):  
Jinjin Chen ◽  
Ren Wang ◽  
Xiao-Fang Li ◽  
Rui-Liang Wang

The aim of the present study was to investigate the effects of Bifidobacterium adolescentis (Bif) supplementation on visceral fat accumulation and insulin sensitivity of the metabolic syndrome in HF-diet-fed rats. Adult male Wistar rats (n 10 per group) were fed four different experimental diets for 12 weeks as follows: standard diet; high-fat (HF) diet; a mix of HF diet and Bif; a mix of standard diet and Bif. Liver, mesenteric fat, epididymal fat, retroperitoneal fat, and inguinal fat, pancreas and triceps surae in all four groups of the rats were weighed, while liver steatosis and insulin sensitivity were evaluated at the end point of the study. As the number of intestinal Bifidobacterium species decreased obviously, fat pad weight and body weight increased significantly in the HF group compared with in the other three groups (P <0·05). Addition of Bif led to a reduction in body weight and fat pad weight (P <0·05). With an increase in liver weight, more severe steatosis of hepatocytes was observed in the HF group compared with in the other three groups. A significant decrease of the glucose infusion rate and pancreas weight was found in the HF group (P <0·05). This deleterious effect was alleviated when Bif was added to the diets. Bifidobacterium supplementation ameliorated visceral fat accumulation and insulin sensitivity of the metabolic syndrome in HF-diet-fed rats.


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