Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome.

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Abstract Text:

Kamal Rahmouni,Melissa A Fath,Seongjin Seo,Daniel R Thedens,Christopher J Berry,Robert Weiss,Darryl Y Nishimura,Val C Sheffield,

Bardet-Biedl syndrome (BBS) is a heterogeneous genetic disorder characterized by many features, including obesity and cardiovascular disease. We previously developed knockout mouse models of 3 BBS genes: BBS2, BBS4, and BBS6. To dissect the mechanisms involved in the metabolic disorders associated with BBS, we assessed the development of obesity in these mouse models and found that BBS-null mice were hyperphagic, had low locomotor activity, and had elevated circulating levels of the hormone leptin. The effect of exogenous leptin on body weight and food intake was attenuated in BBS mice, which suggests that leptin resistance may contribute to hyperleptinemia. In other mouse models of obesity, leptin resistance may be selective rather than systemic; although mice became resistant to leptin's anorectic effects, the ability to increase renal sympathetic nerve activity (SNA) was preserved. Although all 3 of the BBS mouse models were similarly resistant to leptin, the sensitivity of renal SNA to leptin was maintained in Bbs4(-/-) and Bbs6(-/-) mice, but not in Bbs2(-/-) mice. Consequently, Bbs4(-/-) and Bbs6(-/-) mice had higher baseline renal SNA and arterial pressure and a greater reduction in arterial pressure in response to ganglionic blockade. Furthermore, we found that BBS mice had a decreased hypothalamic expression of proopiomelanocortin, which suggests that BBS genes play an important role in maintaining leptin sensitivity in proopiomelanocortin neurons.

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Publishing Authors By Initials

K Rahmouni,MA Fath,S Seo,DR Thedens,CJ Berry,R Weiss,DY Nishimura,VC Sheffield,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of clinical investigation

VOLUME: 118

Page Numbers: 1458-67

Journal Abbreviation: J. Clin. Invest.

ISSN: 0021-9738

DAY: 2

MONTH: Apr

YEAR: 2008

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7802877

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome.

AFFILIATION: Department of Internal Medicine, Department of Pediatrics, Howard Hughes Medical Institute, and Department of Radiology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: J Clin Invest

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome Related Publications

• A knockin mouse model of the Bardet Biedl syndrome 1 M390R mutation has cilia defects, ventriculomegaly, retinopathy, and obesity.
• Ambulance journey records.
• Amniotic fluid embolism.
• Avoidance training and the contiguity principle.
• Determination of ideal PtcO2 measurement time in evaluation of hypoxic wound patients.
• Emetics, cathartics, and gastric lavage.
• Evaluation of the chromosome 2q37.3 gene CENTG2 as an autism susceptibility gene.
• External surface disinfection of the lesser mealworm (Coleoptera: Tenebrionidae).
• Extinction as a function of partial reinforcement and distribution of practice.
• Historical ambient noise levels in a topographically isolated basin.
• Is there a role for metalloproteases in chick neural retina development?
• Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome.
• Longterm follow-up in chondrodysplasia punctata, tibia-metacarpal type, demonstrating natural history.
• Making refractive error services sustainable: the InternationalEye Foundation model.
• Mass Spectroscopic Observation of Shock-Induced Chemistry in Liquid CS(2).
• Molecular cloning and functional expression of rabbit alpha2-antiplasmin.
• Ocular phenotypes of three genetic variants of Bardet-Biedl syndrome.
• Positional cloning of a novel gene on chromosome 16q causing Bardet-Biedl syndrome (BBS2).
• Predictive validity of a functional capacity evaluation: The physical work performance evaluation.
• Preference for a C3 conformation in tris-dimethylaminophosphonium cations: a comparison of the reactions of (Me2N)3P with I-X (X = Cl, Br, I, CN).
• Preliminary studies in the electron microscope of some plant virus inclusion bodies.
• RHEUMATOID ARTHRITIS AND GOUT--A STUDY ON TAIWAN.
• Reversal of adult mental subnormality.
• Safeguarding children: the case for mandatory training.
• Sources of variability in reflectance measurements on normal cadaver ears.
• Spread of effect without reward of learning.
• Surface ultrastructure of mature adult human articular cartilage.
• The appended tail region of heparin cofactor II and additional reactive centre loop mutations combine to increase the reactivity and specificity of alpha1-proteinase inhibitor M358R for thrombin.
• The methylene blue test for bilirubin in urine.
• Unilateral choroidal melanoma with bilateral retinal vasculitis.