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Bovine growth hormone transgenic mice are resistant to diet-induced obesity but develop hyperphagia, dyslipidemia, and diabetes on a high-fat diet

Artikel i vetenskaplig tidskrift
Författare Bob Olsson
Mohammad Bohlooly-Yeganeh
Sharyn M. Fitzgerald
Fredrik Frick
Anna Ljungberg
B. Ahren
Jan Törnell
Göran Bergström
Jan Oscarsson
Publicerad i Endocrinology
Volym 146
Nummer/häfte 2
Sidor 920-30
ISSN 0013-7227 (Print)
Publiceringsår 2005
Publicerad vid Wallenberglaboratoriet
Hjärt-kärlinstitutionen
Institutionen för medicinsk och fysiologisk kemi
Institutionen för invärtesmedicin, Avdelningen för kroppssammansättning och metabolism
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 920-30
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Acromegaly/metabolism/physiopathology, Animals, Body Composition, Body Temperature, Carrier Proteins/genetics, Cattle, Diabetes Mellitus, Experimental/metabolism/*physiopathology, Dietary Fats/pharmacology, Eating, Energy Metabolism/physiology, Glucose Tolerance Test, Growth Hormone/*genetics, Hyperlipidemias/metabolism/*physiopathology, Hyperphagia/metabolism/*physiopathology, Ion Channels, Lipids/blood, Lipoproteins/blood, Membrane Proteins/genetics, Membrane Transport Proteins/genetics, Mice, Mice, Transgenic, Mitochondrial Proteins/genetics, Obesity/metabolism/*physiopathology, Oxygen Consumption/physiology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

It is known that bovine GH (bGH) transgenic mice have increased body mass, insulin resistance, and altered lipoprotein metabolism when fed a normal diet (ND). In this study, the effects of 8 wk of high-fat diet (HFD) were investigated in 6-month-old male bGH mice. Although littermate controls had unchanged energy intake, energy intake was higher in the bGH mice on a HFD than on a low-fat diet. Nevertheless, the bGH mice were resistant to diet-induced weight gain, and only in the bGH mice did the HFD result in increased energy expenditure. Glucose oxidation was higher in the bGH mice compared with littermate controls on both a HFD and ND. In addition, the bGH mice had 0.5 C higher body temperature throughout the day and increased hepatic uncoupling protein 2 expression; changes that were unaffected by the HFD. On a HFD, the effect of bGH overexpression on serum triglycerides and apolipoprotein B was opposite to that on a ND, resulting in higher serum concentrations of triglycerides and apolipoprotein B compared with littermate controls. Increased serum triglycerides were explained by decreased triglyceride clearance. The HFD led to diabetes only in the bGH mice. In conclusion, bGH transgenic mice were resistant to diet-induced obesity despite hyperphagia, possibly due to increased energy expenditure. On a HFD, bGH mice became dyslipidemic and diabetic and thereby more accurately reflect the metabolic situation in acromegalic patients.

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