کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5534305 1550840 2017 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Ablation of PPP1R3G reduces glycogen deposition and mitigates high-fat diet induced obesity
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Ablation of PPP1R3G reduces glycogen deposition and mitigates high-fat diet induced obesity
چکیده انگلیسی


- Reduced glycogen deposition reduces high-fat diet induced obesity in mice.
- Increasing glycogen synthesis elevates lipid accumulation in adipocytes.
- As a glycogen-targeting subunit of PP1, PPP1R3G regulates metabolism in vivo.

Glycogen and triglyceride are two major forms of energy storage in the body and provide the fuel during different phases of food deprivation. However, how glycogen metabolism is linked to fat deposition in adipose tissue has not been clearly characterized. We generated a mouse model with whole-body deletion of PPP1R3G, a glycogen-targeting subunit of protein phosphatase-1 required for glycogen synthesis. Upon feeding with high-fat diet, the body weight and fat composition are significantly reduced in the PPP1R3G−/- mice compared to the wild type controls. The metabolic rate of the mice as measured by O2 consumption and CO2 production is accelerated by PPP1R3G deletion. The high-fat diet-induced liver steatosis is also slightly relieved by PPP1R3G deletion. The glycogen level in adipose tissue is reduced by PPP1R3G deletion. In 3T3L1 cells, overexpression of PPP1R3G leads to increases of both glycogen and triglyceride levels. In conclusion, our study indicates that glycogen is actively involved in fat accumulation in adipose tissue and obesity development upon high-fat diet. Our study also suggests that PPP1R3G is an important player that links glycogen metabolism to lipid metabolism in vivo.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 439, 5 January 2017, Pages 133-140
نویسندگان
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