Journal
HYPERTENSION
Volume 61, Issue 1, Pages 246-+Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.112.201434
Keywords
obesity; glucose intolerance; TRPV1 protein, mouse; mice; hypertension
Categories
Funding
- British Heart Foundation
- Capacity Building Award in Integrative Mammalian Biology
- British Biotechnology Science Research Council
- British Pharmacological Society
- Higher Education Funding Council
- Knowledge Transfer Network
- Medical Research Council
- Scottish Funding Council
- Arthritis Research United Kingdom [19296]
- Diabetes United Kingdom
- BBSRC [BB/E527098/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/E527098/1] Funding Source: researchfish
- British Heart Foundation [PG/12/34/29557] Funding Source: researchfish
Ask authors/readers for more resources
Obesity induced by Western diets is associated with type 2 diabetes mellitus and cardiovascular diseases, although underlying mechanisms are unclear. We investigated a murine model of diet-induced obesity to determine the effect of transient potential receptor vanilloid 1 (TRPV1) deletion on hypertension and metabolic syndrome. Wildtype and TRPV1 knockout mice were fed normal or high-fat diet from 3 to 15 weeks. High-fat diet-fed mice from both genotypes became obese, with similar increases in body and adipose tissue weights. High-fat diet-fed TRPV1 knockout mice showed significantly improved handling of glucose compared with high-fat diet-fed wild-type mice. Hypertension, vascular hypertrophy, and altered nociception were observed in high-fat diet-fed wild-type but not high-fat diet-fed TRPV1 knockout mice. Wild-type, but not high-fat diet-fed TRPV1 knockout, mice demonstrated remodeling in terms of aortic vascular hypertrophy and increased heart and kidney weight, although resistance vessel responses were similar in each. Moreover, the wild-type mice had significantly increased plasma levels of leptin, interleukin 10 and interleukin 1 beta, whereas samples from TRPV1 knockout mice did not show significant increases. Our results do not support the concept that TRPV1 plays a major role in influencing weight gain. However, we identified a role of TRPV1 in the deleterious effects observed with high-fat feeding in terms of inducing hypertension, impairing thermal nociception sensitivity, and reducing glucose tolerance. The observation of raised levels of adipokines in wild-type but not TRPV1 knockout mice is in keeping with TRPV1 involvement in stimulating the proinflammatory network that is central to obesity-induced hypertension and sensory neuronal dysfunction. (Hypertension. 2013;61:246-252.). center dot Online Data Supplement
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available