Regulation of mouse sterol regulatory element-binding protein-1c gene (SREBP-1c) by oxysterol receptors, LXR(alpha) and LXR(beta)

Article Abstract:

The liver X receptors (LXRs), members of the nuclear hormone receptor superfamily bound and activated by oxysterols, are discussed. Regulation of mouse sterol regulatory element-binding protein-1c gene (SREBP-1c) by LXR(alpha) and LXR(beta) has been studied. Findings show a unique regulatory relationship between cholesterol and fatty acid metabolism.

Liver, Mice, Mice (Rodents), Genetic regulation, Gene expression, Genetic transcription, Transcription (Genetics), Sterols

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Role of LXRs in control of lipogenesis

Article Abstract:

The role of liver X receptors (LXRs) in the control of lipogenesis is discussed. A nonsteroidal LXR agonist and its analog have been identified and the biochemical features have been investigated. Studies of a complementary nature have yielded data that suggest that increase in plasma lipids comes though LXR-mediated induction of the sterol regulatory element-binding protein1 (SREBP-1) lipogenic process. It appears the hypertriglyceridemic effect is associated.

Usage, Mice, mutant strains, Mutant mice, Hydroxylases, Triglycerides

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Insulin resistance and diabetes mellitus in transgenic mice expressing nuclear SREBP-1c in adipose tissue: model for congenital generalized lipodystrophy

Article Abstract:

When the nuclear type of sterol regulatory element-binding protein-1c (nSREBP-1c/ADD1) is overexpressed in cultured 3T3-LI preadipocytes, adipocyte differentiation occurs. Transgenic mice with overexpression of nSREBP-1c in fat tissue have been produced under regulation of the adipocyte-specific aP2 enhancer/promoter. Disordered differentiation of fat tissue, insulin resistance of significance, diabetes mellitus and fatty liver from birth, with high plasma triglyceride levels later, were seen in a syndrome. Mice of this type have many of the same things seen in congenital generalized lipodystrophy (CGL).

Diabetes, Diabetes mellitus, Observations, Protein binding, Adipose tissues, Adipose tissue, Insulin resistance, Genetically modified mice

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