RGD Reference Report - Complement Factor B Is a Determinant of Both Metabolic and Cardiovascular Features of Metabolic Syndrome. - Rat Genome Database

RGD Reference Report - Complement Factor B Is a Determinant of Both Metabolic and Cardiovascular Features of Metabolic Syndrome. - Rat Genome Database

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General

Complement Factor B Is a Determinant of Both Metabolic and Cardiovascular Features of Metabolic Syndrome.
Authors:	Coan, Philip M Barrier, Marjorie Alfazema, Neza Carter, Roderick N Marion de Procé, Sophie Dopico, Xaquin C Garcia Diaz, Ana Thomson, Adrian Jackson-Jones, Lucy H Moyon, Ben Webster, Zoe Ross, David Moss, Julie Arends, Mark J Morton, Nicholas M Aitman, Timothy J
Citation:	Coan PM, etal., Hypertension. 2017 Jul 24. pii: HYPERTENSIONAHA.117.09242. doi: 10.1161/HYPERTENSIONAHA.117.09242.
RGD ID:	127285403
Pubmed:	PMID:28739975 (View Abstract at PubMed)
PMCID:	PMC5548512 (View Article at PubMed Central)
DOI:	DOI:10.1161/HYPERTENSIONAHA.117.09242 (Journal Full-text)
CFB (complement factor B) is elevated in adipose tissue and serum from patients with type 2 diabetes mellitus and cardiovascular disease, but the causal relationship to disease pathogenesis is unclear. Cfb is also elevated in adipose tissue and serum of the spontaneously hypertensive rat, a well-characterized model of metabolic syndrome. To establish the role of CFB in metabolic syndrome, we knocked out the Cfb gene in the spontaneously hypertensive rat. Cfb -/- rats showed improved glucose tolerance and insulin sensitivity, redistribution of visceral to subcutaneous fat, increased adipocyte mitochondrial respiration, and marked changes in gene expression. Cfb -/- rats also had lower blood pressure, increased ejection fraction and fractional shortening, and reduced left ventricular mass. These changes in metabolism and gene expression, in adipose tissue and left ventricle, suggest new adipose tissue-intrinsic and blood pressure-independent mechanisms for insulin resistance and cardiac hypertrophy in the spontaneously hypertensive rat. In silico analysis of the human CFB locus revealed 2 cis-regulated expression quantitative trait loci for CFB expression significantly associated with visceral fat, circulating triglycerides and hypertension in genome-wide association studies. Together, these data demonstrate a key role for CFB in the development of spontaneously hypertensive rat metabolic syndrome phenotypes and of related traits in humans and indicate the potential for CFB as a novel target for treatment of cardiometabolic disease.

Annotation Click to see Annotation Detail View

Phenotype Annotations

Mammalian Phenotype

decreased brown adipose tissue amount (IMP)

decreased circulating aldosterone level (IMP)

decreased circulating cholesterol level (IMP)

decreased circulating interferon-gamma level (IMP)

decreased circulating interleukin-10 level (IMP)

decreased epididymal fat pad weight (IMP)

decreased fasting circulating glucose level (IMP)

decreased mesenteric fat pad weight (IMP)

decreased retroperitoneal fat pad weight (IMP)

decreased systemic arterial systolic blood pressure (IMP)

decreased triglyceride level (IMP)

increased insulin sensitivity (IMP)

increased subcutaneous adipose tissue amount (IMP)

Objects Annotated

Genes (Rattus norvegicus)

Cfb (complement factor B)

Cfb^em1Tja (complement factor B, ZFN induced mutant 1, Tja)

Strains

SHR-Cfb^em1Tja (NA)

Additional Information