Filtered By:
Condition: Diabetes Type 2

This page shows you your search results in order of date. This is page number 10.

Order by Relevance | Date

Total 421 results found since Jan 2013.

Resolvin D3 improves the impairment of insulin signaling in skeletal muscle and nonalcoholic fatty liver disease through AMPK/autophagy-associated attenuation of ER stress
Biochem Pharmacol. 2022 Aug 7;203:115203. doi: 10.1016/j.bcp.2022.115203. Online ahead of print.ABSTRACTResolvin D3 (RD3), an endogenous lipid mediator derived from omega-3 fatty acids, has been documented to attenuate inflammation in various disease models. Although it has been reported that omega-3 fatty acids attenuate metabolic disorders, the roles of RD3 in insulin signaling in skeletal muscle and hepatic lipid metabolism remain unclear. In the current study, we examined the role of RD3 in skeletal muscle insulin resistance and hepatic steatosis using in vitro and in vivo obesity models. In mouse primary hepatocytes, ...
Source: Biochemical Pharmacology - August 10, 2022 Category: Drugs & Pharmacology Authors: Heeseung Oh Wonjun Cho A M Abd El-Aty Cemil Bayram Ji Hoon Jeong Tae Woo Jung Source Type: research

H19 inhibition increases HDAC6 and regulates IRS1 levels and insulin signaling in the skeletal muscle during diabetes
CONCLUSIONS: Our results suggest a critical role for the lncRNA H19-HDAC6 axis in regulating IRS1 levels in the skeletal muscle during diabetes and therefore restoring normal H19 levels might hold a therapeutic potential for the management of aberrant skeletal muscle physiology during insulin resistance and type 2 diabetes.PMID:35842608 | DOI:10.1186/s10020-022-00507-3
Source: Molecular Medicine - July 16, 2022 Category: Molecular Biology Authors: Amit Kumar Malabika Datta Source Type: research

Gasdermin D is involved in switching from apoptosis to pyroptosis in TLR4-mediated renal tubular epithelial cells injury in diabetic kidney disease
CONCLUSIONS: TLR4 could exacerbate tubular injury and fibrosis via GSDMD-mediated canonical pyroptosis pathway in T2DKD. Activation of GSDMD could inhibit apoptosis and activate pyroptosis, which may involve the potential switch mechanism between TLR4-mediated pyroptosis and apoptosis in T2DKD.PMID:35809639 | DOI:10.1016/j.abb.2022.109347
Source: Archives of Biochemistry and Biophysics - July 9, 2022 Category: Biochemistry Authors: Shuguang Yuan Youliang Wang Zheng Li Xiaojun Chen Panai Song Anqun Chen Zhong Qu Si Wen Hong Liu Xuejing Zhu Source Type: research

SIRT3 attenuates coronary atherosclerosis in diabetic patients by regulating endothelial cell function
CONCLUSION: SIRT3 was associated with the progression of atherosclerosis in T2DM patients through upregulation of PPAR-α and eNOS and downregulation of iNOS, which are involved in endothelial dysfunction under hyperglycemic conditions.PMID:35791925 | DOI:10.1002/jcla.24586
Source: Atherosclerosis - July 6, 2022 Category: Cardiology Authors: Huiping Gong Jing Liu Zhiwei Xue Wenwen Wang Cuicui Li Fanfan Xu Yimeng Du Xiaona Lyu Source Type: research

Lauric acid impairs insulin-induced Akt phosphorylation by upregulating SELENOP expression via HNF4 α induction
Am J Physiol Endocrinol Metab. 2022 May 2. doi: 10.1152/ajpendo.00163.2021. Online ahead of print.ABSTRACTSelenoprotein P (SeP; encoded by SELENOP in humans, Selenop in rodents) is a hepatokine that is upregulated in the liver of humans with type 2 diabetes. Excess SeP contributes to the onset of insulin resistance and various type 2 diabetes-related complications. We have previously reported that the long-chain saturated fatty acid, palmitic acid, upregulates Selenop expression, whereas the polyunsaturated fatty acids (PUFAs) downregulate it in hepatocytes. However, the effect of medium-chain fatty acids (MCFAs) on Seleno...
Source: Am J Physiol Endocri... - May 2, 2022 Category: Endocrinology Authors: Kyoko Kamoshita Hirohiko Tsugane Kiyo-Aki Ishii Hiroaki Takayama Xingyu Yao Halimulati Abuduwaili Ryota Tanida Yasumasa Taniguchi Hein Ko Oo Guzel Gafiyatullina Shuichi Kaneko Seiichi Matsugo Toshinari Takamura Source Type: research