Visceral fat: higher responsiveness of fat mass and gene expression to calorie restriction than subcutaneous fat.
Visceral fat accumulation is accompanied by several metabolic disorders. Here, we investigate the improvement of visceral fat accumulation in the early phase of diet. Hyperlipidemic obese patients received a low-calorie diet (1000 kcal/day) for 14 days. Visceral and subcutaneous fat accumulation was analyzed using ultrasonography. After 14 days of the diet, the average visceral fat of obese patients obviously decreased (P < 0.05), as well as the visceral fat-related secreted proteins, whereas subcutaneous fat did not decrease in these patients. These results show that visceral fat is reduced significantly in the early phase of diet therapy in humans. Therefore, to clarify its mechanism, we analyzed the expression of lipid metabolism-related genes in visceral and subcutaneous fat using obese rats. The Long-Evans Tokushima Otsuka (LETO) rats, as an obese model, were divided into two groups: fasting and non-fasting. The gene expressions in visceral and subcutaneous fat were measured by reverse transcriptase-polymerase chain reaction (RT-PCR). The expression of beta(3)-adrenergic receptor (AR), hormone sensitive lipase (HSL), peroxisome proliferator-activated receptor (PPAR)-gamma, and uncoupling protein (UCP)-2 genes increased by 3.2-, 2.3-, 2.2-, and 2-fold in visceral fat (P < 0.01), but remained almost unchanged in subcutaneous fat. Taken together, the responsiveness of lipid metabolism-related genes to fasting is more sensitive in visceral fat than in subcutaneous fat in rats, suggesting that the different responsiveness to calorie restriction in fat tissues is due to the different induction of metabolism-related gene expression.
Li
Yin
Y
Department of Clinical Cell Biology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Bujo
Hideaki
H
Takahashi
Kazuo
K
Shibasaki
Manabu
M
Zhu
Yanjuan
Y
Yoshida
Yuriko
Y
Otsuka
Yuko
Y
Hashimoto
Naotake
N
Saito
Yasushi
Y
D000273:Adipose Tissue / Q000378:metabolism / Q000502:physiology*; D000328:Adult; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001823:Body Composition; D031204:Caloric Restriction; D004195:Disease Models, Animal; D005215:Fasting / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D006949:Hyperlipidemias / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins; D007473:Ion Channels; D008297:Male; D026901:Membrane Transport Proteins; D008875:Middle Aged; D024101:Mitochondrial Proteins; D056918:Nuclear Receptor Coactivators; D009765:Obesity / Q000378:metabolism; D014176:Protein Biosynthesis; D011506:Proteins / Q000235:genetics; D051381:Rats; D020334:Rats, Inbred OLETF; D022702:Receptors, Adrenergic, beta-3 / Q000096:biosynthesis / Q000235:genetics; D002787:Sterol Esterase / Q000096:biosynthesis / Q000235:genetics; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics; D000071246:Uncoupling Protein 2
D015415:Biomarkers; D047908:Intracellular Signaling Peptides and Proteins; D007473:Ion Channels; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; C486559:NCOA6 protein, human; C486560:Ncoa6 protein, rat; D056918:Nuclear Receptor Coactivators; D011506:Proteins; D022702:Receptors, Adrenergic, beta-3; D014157:Transcription Factors; C000604389:UCP2 protein, human; C000604391:Ucp2 protein, rat; D000071246:Uncoupling Protein 2; D002787:Sterol Esterase