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Mature-onset obesity in interleukin-1 receptor I knockout mice.

Artikel i vetenskaplig tidskrift
Författare Maria C García
Ingrid Wernstedt
Anna Berndtsson
Maria Enge
Michal Bell
Olof H. Hultgren
Michael Horn
Bo Ahrén
Sven Enerbäck
Claes Ohlsson
Ville Wallenius
John-Olov Jansson
Publicerad i Diabetes
Volym 55
Nummer/häfte 5
Sidor 1205-13
ISSN 0012-1797
Publiceringsår 2006
Publicerad vid Wallenberglaboratoriet
Institutionen för biomedicin, avdelningen för medicinsk genetik och klinisk genetik
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för medicin, avdelningen för invärtesmedicin
Institutionen för kliniska vetenskaper
Sidor 1205-13
Språk en
Länkar dx.doi.org/10.2337/db05-1304
Ämnesord Adipose Tissue, anatomy & histology, Aging, Animals, Body Weight, Densitometry, X-Ray, Leptin, blood, pharmacology, Mice, Mice, Knockout, Obesity, blood, genetics, Organ Size, Receptors, Interleukin-1, deficiency, genetics, physiology
Ämneskategorier Farmakologi, Molekylär medicin (genetik och patologi), Diabetologi

Sammanfattning

Interleukin-1 (IL-1) is a major mediator of inflammation that exerts its biological activities through the IL-1 type I receptor (IL-1RI). The body weights of IL-1RI(-/-) mice of both sexes started to deviate from those of wild-type mice at 5-6 months of age and were 20% higher at 9 months of age. Visceral and subcutaneous fat mass, measured by dual-energy X-ray absorptiometry and magnetic resonance imaging, was markedly (1.5- to 2.5-fold) increased. Lean body mass and crown-rump length were also slightly (11 and 5%, respectively) increased, as was serum IGF-I. Obese IL-1RI(-/-) mice were insulin resistant, as evidenced by hyperinsulinemia, decreased glucose tolerance, and insulin sensitivity. To elucidate the mechanisms for the development of obesity, young pre-obese IL-1RI(-/-) mice were investigated. They showed decreased suppression of body weight and food intake in response to systemic leptin treatment. The decreased leptin responsiveness was even more pronounced in older obese animals. Moreover, spontaneous locomotor activity and fat utilization, as measured by respiratory quotient, were decreased in pre-obese IL-1RI(-/-) mice. In conclusion, lack of IL-1RI-mediated biological activity causes mature-onset obesity. This obese phenotype is preceded by decreased leptin sensitivity, fat utilization, and locomotor activity.

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