Key result
Grp78 heterozygosity in male mice increased energy expenditure and attenuated high-fat diet-induced obesity, hyperinsulinemia, liver steatosis, and hyperglycemia.
Why the study?
Does Grp78 heterozygosity attenuate diet-induced obesity and insulin resistance in mice on a high-fat diet?
Population
Male Grp78(+/-) mice and their wild-type littermates
Comparison
Grp78 heterozygosity (Grp78) combined with a… vs Wild-type littermates on a high-fat diet (HFD)
Design
Preclinical
Authors
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May support Grp78 as a metabolic target in male mice; hypothesis-generating and should not yet inform human practice.
Does Grp78 heterozygosity attenuate diet-induced obesity and insulin resistance in mice on a high-fat diet?
Grp78 heterozygosity protects against high-fat diet-induced obesity and insulin resistance by promoting an adaptive unfolded protein response in white adipose tissue.
Ye et al. (2009) studied obesity, insulin resistance, and type 2 diabetes. Grp78 heterozygosity vs. wild-type littermates was evaluated on obesity, insulin resistance, and type 2 diabetes pathogenesis. Grp78 heterozygosity in male mice increased energy expenditure and attenuated high-fat diet-induced obesity, hyperinsulinemia, liver steatosis, and hyperglycemia.
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