2008
DOI: 10.1007/s00125-008-0969-0
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Abstract: To the Editor: Obesity is associated with insulin resistance and type 2 diabetes, with accumulation of intra-abdominal fat carrying a more severe disease risk than accumulation of subcutaneous fat. It remains unclear whether increased visceral fat has an adverse metabolic effect due to its location or to the unique properties of intra-abdominal adipocytes. Konrad et al. [1] reported that increasing intra-abdominal fat mass by transplantation of epididymal fat from normal mice into lean recipients improved fast… Show more

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Cited by 69 publications
(80 citation statements)
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“…Most importantly from a clinical perspective, peripheral Y1-receptor knockdown protected against high fat diet-induced increases in body weight and total adiposity in the absence of effects on lean mass or inguinal fat mass. As preservation of lean mass and inguinal fat during loss of excess adiposity is desirable because of known beneficial effects of these tissues on metabolic rate and disease risk, [54][55][56][57][58] and as these benefits could be achieved without the need to deliver Y1 antagonists to the brain, this finding has significant implications for the pharmacological management of obesity. The increased fat oxidation seen in Y1-deficient mice is likely mediated by increased capacity for fatty acid transport into mitochondria and increased b-oxidation.…”
Section: Discussionmentioning
confidence: 99%
“…Most importantly from a clinical perspective, peripheral Y1-receptor knockdown protected against high fat diet-induced increases in body weight and total adiposity in the absence of effects on lean mass or inguinal fat mass. As preservation of lean mass and inguinal fat during loss of excess adiposity is desirable because of known beneficial effects of these tissues on metabolic rate and disease risk, [54][55][56][57][58] and as these benefits could be achieved without the need to deliver Y1 antagonists to the brain, this finding has significant implications for the pharmacological management of obesity. The increased fat oxidation seen in Y1-deficient mice is likely mediated by increased capacity for fatty acid transport into mitochondria and increased b-oxidation.…”
Section: Discussionmentioning
confidence: 99%
“…By contrast, expansion of subcutaneous WAT, even in the setting of obesity, has been suggested to promote insulin sensitivity in rodents and humans (9)(10)(11)(12)(13)(14). Implantation of subcutaneous WAT, but not visceral WAT, into the abdominal cavity of mice improves whole-body metabolism (15,16). Moreover, subcutaneous and visceral WAT express unique gene signatures (17).…”
Section: Introductionmentioning
confidence: 99%
“…Lacy and Bartness (30) reported that Siberian hamsters do not reduce body fat to compensate for dorsal subcutaneous fat transplants, and Foster et al (10) reported no compensation for intra-abdominal fat transplants in rats. Hocking et al (25) found that transplants of subcutaneous fat into the intra-abdominal space reduced the size of endogenous fat depots in male mice, but transplanting intra-abdominal fat subcutaneously did not. Therefore, there appears to be a complex interaction between the source of the transplant, the site at which the transplant is placed, and the species or strain of the animal that determines whether or not a recipient compensates for transplanted fat.…”
Section: Discussionmentioning
confidence: 99%