scholarly journals Correction to: Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Zhi-Hong Yang ◽  
Hiroko Miyahara ◽  
Akimasa Hatanaka
2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Tina Schumann ◽  
Jörg König ◽  
Christian von Loeffelholz ◽  
Daniel F. Vatner ◽  
Dongyan Zhang ◽  
...  

AbstractGenome-wide association studies have identified SLC16A13 as a novel susceptibility gene for type 2 diabetes. The SLC16A13 gene encodes SLC16A13/MCT13, a member of the solute carrier 16 family of monocarboxylate transporters. Despite its potential importance to diabetes development, the physiological function of SLC16A13 is unknown. Here, we validate Slc16a13 as a lactate transporter expressed at the plasma membrane and report on the effect of Slc16a13 deletion in a mouse model. We show that Slc16a13 increases mitochondrial respiration in the liver, leading to reduced hepatic lipid accumulation and increased hepatic insulin sensitivity in high-fat diet fed Slc16a13 knockout mice. We propose a mechanism for improved hepatic insulin sensitivity in the context of Slc16a13 deficiency in which reduced intrahepatocellular lactate availability drives increased AMPK activation and increased mitochondrial respiration, while reducing hepatic lipid content. Slc16a13 deficiency thereby attenuates hepatic diacylglycerol-PKCε mediated insulin resistance in obese mice. Together, these data suggest that SLC16A13 is a potential target for the treatment of type 2 diabetes and non-alcoholic fatty liver disease.


PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e53094 ◽  
Author(s):  
Lisa Kolden Midtbø ◽  
Mohammad Madani Ibrahim ◽  
Lene Secher Myrmel ◽  
Ulrike Liisberg Aune ◽  
Anita Røyneberg Alvheim ◽  
...  

2019 ◽  
Vol 122 (6) ◽  
pp. 616-624 ◽  
Author(s):  
Yu Niu ◽  
Jintian He ◽  
Hussain Ahmad ◽  
Chao Wang ◽  
Xiang Zhong ◽  
...  

AbstractThe objective of the present study was to investigate the effect of curcumin on insulin resistance (IR) and hepatic lipid accumulation in intra-uterine growth restriction (IUGR). Rats with a normal birth weight (NBW) or IUGR were fed basic diets (NBW and IUGR groups) or basic diets supplemented with curcumin (NBW-C and IUGR-C groups) from 6 to 12 weeks. Rats in the IUGR group showed higher levels of glucose and homeostasis model assessment for insulin resistance index (HOMA-IR) (P< 0·05) than in the NBW group. The livers of IUGR rats exhibited higher (P< 0·05) concentration of TAG and lower (P< 0·05) activities of lipolysis enzymes compared with the normal rats. In response to dietary curcumin supplementation, concentrations of serum insulin, glucose and HOMA-IR, pyruvate, TAG, total cholesterol and NEFA in the liver were decreased (P< 0·05). The concentrations of glycogen and activities of lipolysis enzymes in the liver were increased (P< 0·05) in the IUGR-C group compared with the IUGR group. These results were associated with lower (P< 0·05) phosphorylated insulin receptor substrate 1, protein kinase B or Akt, glycogen synthase kinase 3β and expressions of sterol regulatory element binding protein 1 and fatty acid synthase (FASN); decreased expressions forCd36, sterol regulatory element binding protein 1c (Srebf1) andFasn; increased (P< 0·05) expression of PPARα; and expressions forPparaand hormone-sensitive lipase in the liver of IUGR-C rats than the IUGR rats. Maternal malnutrition caused IR and lipid accumulation in the liver. Curcumin supplementation prevented IR by regulating insulin signalling pathways and attenuated hepatic lipid accumulation.


2013 ◽  
Vol 61 (18) ◽  
pp. 4371-4378 ◽  
Author(s):  
Aidilla Mubarak ◽  
Jonathan M. Hodgson ◽  
Michael J. Considine ◽  
Kevin D. Croft ◽  
Vance B. Matthews

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Zhan Liu ◽  
Peng Li ◽  
Zhi-Hong Zhao ◽  
Yu Zhang ◽  
Zhi-Min Ma ◽  
...  

Backgrounds.VitB6 deficiency has been associated with a number of adverse health effects. However, the effects of VitB6 in metabolic syndrome are poorly understood.Methods.VitB6 (50 mg/kg/day) was given toApoe-/-mice with hkdigh-fat diet (HFD) for 8 weeks. Endothelial dysfunction, insulin resistance, and hepatic lipid contents were determined.Results.VitB6 administration remarkably increased acetylcholine-induced endothelium-dependent relaxation and decreased random blood glucose level inApoe-/-mice fed with HFD. In addition, VitB6 improved the tolerance of glucose and insulin, normalized the histopathology of liver, and reduced hepatic lipid accumulation but did not affect the liver functions. Clinical and biochemical analysis indicated that the levels of VitB6 were decreased in patients with fatty liver.Conclusions.Vitamin B6 prevents endothelial dysfunction, insulin resistance, and hepatic lipid accumulation inApoe-/-mice fed with HFD. Supplementation of VitB6 should be considered to prevent metabolic syndrome.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1751-P
Author(s):  
CHIEN-NING HUANG ◽  
HSIN-HUA LI ◽  
CHIUNG-HUEI PENG ◽  
EDY KORNELIUS ◽  
YI SUN YANG ◽  
...  

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