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Specialty: Biomedical Science
Condition: Metabolic Syndrome

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Total 3 results found since Jan 2013.

Lipopolysaccharide promoted proliferation and adipogenesis of preadipocytes through JAK/STAT and AMPK-regulated cPLA2 expression.
Authors: Chang CC, Sia KC, Chang JF, Lin CM, Yang CM, Huang KY, Lin WN Abstract The proliferation and adipogenesis of preadipocytes played important roles in the development of adipose tissue and contributed much to the processes of obesity. On the other hand, lipopolysaccharide (LPS), also known as endotoxin, is a key outer membrane component of gram-negative bacteria in the gut microbiota, and has a dominant role in linking inflammation to high-fat diet-induced metabolic syndrome. Studies suggested the potential roles of LPS in hepatic steatosis and in obese mice models. However, the molecular mechanisms underlyi...
Source: International Journal of Medical Sciences - January 22, 2019 Category: Biomedical Science Tags: Int J Med Sci Source Type: research

CREG1 heterozygous mice are susceptible to high fat diet-induced obesity and insulin resistance
This study uncovered a novel function of CREG1 in metabolic disorders.
Source: PLoS One - May 1, 2017 Category: Biomedical Science Authors: Xiaoxiang Tian Source Type: research

Dual effects of fructose on ChREBP and FoxO1/3{alpha} are responsible for AldoB upregulation and vascular remodeling
Increased production of methylglyoxal (MG) in vascular tissues is one of the causative factors for vascular remodeling in different subtypes of metabolic syndrome, including hypertension and insulin resistance. Fructose-induced upregulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms have been unclear. Serum levels of MG and fructose were determined in diabetic patients with hypertension. MG level had significant positive correlations with blood pressure and fructose level respectively. C57Bl/6 mice were fed with control or fructose-enriched diet for 3 months and ultr...
Source: Clinical Science - December 21, 2016 Category: Biomedical Science Authors: Cao, W., Chang, T., Li, X.-q., Wang, R., Wu, L. Tags: PublishAheadOfPrint Source Type: research