scholarly journals Clusterin Impairs Hepatic Insulin Sensitivity and Adipocyte Clusterin Associates With Cardiometabolic Risk

Diabetes Care ◽  
2019 ◽  
Vol 42 (3) ◽  
pp. 466-475 ◽  
Author(s):  
David Bradley ◽  
Alecia Blaszczak ◽  
Zheng Yin ◽  
Joey Liu ◽  
Joshua J. Joseph ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Cardiometabolic Risk ◽  
Hepatic Insulin Sensitivity

Lower Hepatic Insulin Sensitivity in a Family with a Recently Described Glucokinase Gene Variant

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1509-P ◽  
Author(s):  
KÁLMÁN BÓDIS ◽  
OANA P. ZAHARIA ◽  
YANISLAVA KARUSHEVA ◽  
PAVEL BOBROV ◽  
DANIEL F. MARKGRAF ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Gene Variant ◽  
Glucokinase Gene ◽  
Hepatic Insulin Sensitivity

Exenatide Treatment Improves Mitochondrial Metabolism and Hepatic Insulin Sensitivity in Mice with Nonalcoholic Steatohepatitis (NASH)

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1846-P
Author(s):  
SRILAXMI KALAVALAPALLI ◽  
FERNANDO BRIL ◽  
ARIANA VERGARA ◽  
NISHANTH SUNNY ◽  
KENNETH CUSI
Keyword(s):  
Insulin Sensitivity ◽  
Nonalcoholic Steatohepatitis ◽  
Mitochondrial Metabolism ◽  
Hepatic Insulin Sensitivity

Regulation of Hepatic Insulin Sensitivity and Hepatic Steatosis by ULK1

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1863-P ◽  
Author(s):  
YOUNGDO KOO ◽  
MICHAEL P. GARNEAU ◽  
QUANJIANG ZHANG ◽  
E. DALE ABEL
Keyword(s):  
Insulin Sensitivity ◽  
Hepatic Steatosis ◽  
Hepatic Insulin Sensitivity

scholarly journals Regulation of Mitochondria-Associated Membranes (MAMs) by NO/sGC/PKG Participates in the Control of Hepatic Insulin Response

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1319 ◽  
Author(s):  
Arthur Bassot ◽  
Marie-Agnès Chauvin ◽  
Nadia Bendridi ◽  
Jingwei Ji-Cao ◽  
Guillaume Vial ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Soluble Guanylate Cyclase ◽  
Insulin Response ◽  
Cyclophilin D ◽  
Hepatic Insulin Sensitivity ◽  
Physiological Conditions ◽  
Huh7 Cells ◽  
The Impact

Under physiological conditions, nitric oxide (NO) produced by the endothelial NO synthase (eNOS) upregulates hepatic insulin sensitivity. Recently, contact sites between the endoplasmic reticulum and mitochondria named mitochondria-associated membranes (MAMs) emerged as a crucial hub for insulin signaling in the liver. As mitochondria are targets of NO, we explored whether NO regulates hepatic insulin sensitivity by targeting MAMs. In Huh7 cells, primary rat hepatocytes and mouse livers, enhancing NO concentration increased MAMs, whereas inhibiting eNOS decreased them. In vitro, those effects were prevented by inhibiting protein kinase G (PKG) and mimicked by activating soluble guanylate cyclase (sGC) and PKG. In agreement with the regulation of MAMs, increasing NO concentration improved insulin signaling, both in vitro and in vivo, while eNOS inhibition disrupted this response. Finally, inhibition of insulin signaling by wortmannin did not affect the impact of NO on MAMs, while experimental MAM disruption, using either targeted silencing of cyclophilin D or the overexpression of the organelle spacer fetal and adult testis-expressed 1 (FATE-1), significantly blunted the effects of NO on both MAMs and insulin response. Therefore, under physiological conditions, NO participates to the regulation of MAM integrity through the sGC/PKG pathway and concomitantly improves hepatic insulin sensitivity. Altogether, our data suggest that the induction of MAMs participate in the impact of NO on hepatocyte insulin response.

scholarly journals Measurement of hepatic insulin sensitivity early after the bypass of the proximal small bowel in humans

2016 ◽  
Vol 3 (1) ◽  
pp. 95-98 ◽  
Author(s):  
A. D. Miras ◽  
R. Herring ◽  
A. Vusirikala ◽  
F. Shojaee‐Moradi ◽  
N. C. Jackson ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Small Bowel ◽  
Hepatic Insulin Sensitivity ◽  
Proximal Small Bowel

scholarly journals Short-term strength training reduces gluconeogenesis and NAFLD in obese mice

2019 ◽  
Vol 241 (1) ◽  
pp. 59-70 ◽  
Author(s):  
Rodrigo Martins Pereira ◽  
Kellen Cristina da Cruz Rodrigues ◽  
Chadi Pellegrini Anaruma ◽  
Marcella Ramos Sant’Ana ◽  
Thaís Dantis Pereira de Campos ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Strength Training ◽  
Term Strength ◽  
Obese Mice ◽  
Short Term ◽  
Fat Accumulation ◽  
Hepatic Insulin Sensitivity ◽  
Short Term Strength ◽  
Hepatic Fat

Non-alcoholic fatty liver disease (NAFLD) has a positive correlation with obesity, insulin resistance and type 2 diabetes mellitus (T2D). The aerobic training is an important tool in combating NAFLD. However, no studies have demonstrated the molecular effects of short-term strength training on the accumulation of hepatic fat in obese mice. This study aimed to investigate the effects of short-term strength training on the mechanisms of oxidation and lipid synthesis in the liver of obese mice. The short duration protocol was used to avoid changing the amount of adipose tissue. Swiss mice were separated into three groups: lean control (CTL), sedentary obese (OB) and strength training obese (STO). The obese groups were fed a high-fat diet (HFD) and the STO group performed the strength training protocol 1 session/day for 15 days. The short-term strength training reduced hepatic fat accumulation, increasing hepatic insulin sensitivity and controlling hepatic glucose production. The obese animals increased the mRNA of lipogenic genes Fasn and Scd1 and reduced the oxidative genes Cpt1a and Ppara. On the other hand, the STO group presented the opposite results. Finally, the obese animals presented higher levels of lipogenic proteins (ACC and FAS) and proinflammatory cytokines (TNF-α and IL-1β), but the short-term strength training was efficient in reducing this condition, regardless of body weight loss. In conclusion, there was a reduction of obesity-related hepatic lipogenesis and inflammation after short-term strength training, independent of weight loss, leading to improvements in hepatic insulin sensitivity and glycemic homeostasis in obese mice. Key points: (1) Short-term strength training (STST) reduced fat accumulation and inflammation in the liver; (2) Hepatic insulin sensitivity and HPG control were increased with STST; (3) The content and activity of ACC and content of FAS were reduced with STST; (4) STST improved hepatic fat accumulation and glycemic homeostasis; (5) STST effects were observed independently of body weight change.

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