Transplantation or removal of intra-abdominal adipose tissue prevents age-induced glucose insensitivity

Foster, Michelle T.; Shi, Haifei; Seeley, Randy J.; Woods, Stephen C.

doi:10.1016/j.physbeh.2010.05.014

Cited by 35 publications

(34 citation statements)

References 39 publications

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“…To determine if C57Bl6/J mice display similar phenotypes in the high-fat diet (HFD) model of obesity, we measured whole body fat mass (Figure 1A) and fat pad weight of the perigonadal VWAT and the inguinal SWAT depots (Figure 1B) after 8 weeks of HFD or standard diet (SD) feeding. Although the precise anatomic location of these depots in mice differ from humans, these mouse depots impact metabolism similarly to human visceral adipose tissues (Barzilai et al, 1999; Foster et al, 2010, 2011; Gabriely and Barzilai, 2003) and gluteofemoral adipose tissue (Foster et al, 2013; Tran et al, 2008), respectively. We find that upon HFD feeding, males accumulate more fat mass than females (Figure 1A), consistent with previous reports (Grove et al, 2010; Medrikova et al, 2012).…”

Section: Resultsmentioning

confidence: 99%

The Adipose Tissue Microenvironment Regulates Depot-Specific Adipogenesis in Obesity

et al. 2016

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Summary The sexually dimorphic distribution of adipose tissue influences the development of obesity-associated pathologies. The accumulation of visceral white adipose tissue (VWAT) that occurs in males is detrimental to metabolic health, while accumulation of subcutaneous adipose tissue (SWAT) seen in females may be protective. Here, we show that adipocyte hyperplasia contributes directly to the differential fat distribution between the sexes. In male mice, high-fat diet (HFD) induces adipogenesis specifically in VWAT, while in females HFD induces adipogenesis in both VWAT and SWAT in a sex hormone-dependent manner. We also show that the activation of adipocyte precursors (APs), which drives adipocyte hyperplasia in obesity, is regulated by the adipose depot microenvironment and not by cell-intrinsic mechanisms. These findings indicate that APs are plastic cells, which respond to both local and systemic signals that influence their differentiation potential independent of depot origin. Therefore, depot-specific AP microenvironment niches coordinate adipose tissue growth and distribution.

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Section: Resultsmentioning

confidence: 99%

The Adipose Tissue Microenvironment Regulates Depot-Specific Adipogenesis in Obesity

et al. 2016

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“…Adipose tissue removal in humans 18,23,24 and rodents 30,35 induces compensation in remaining nonexcised adipose tissue depots. Rodent studies demonstrate that compensatory adipose depot mass differences are not detectable 5 weeks post-surgery, 55 but significant compensatory redistribution of lipids to non-excised adipose depots occurs »12 weeks post-surgery. The extent of compensation differs according to the depot removed, hence intra-abdominal adipose tissue depot removal (i.e., epididymal) significantly increases mass of non-excised adipose depots, whereas inguinal does not.…”

Section: Discussionmentioning

confidence: 99%

Lower body adipose tissue removal decreases glucose tolerance and insulin sensitivity in mice with exposure to high fat diet

et al. 2014

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MT Foster (2015) Lower body adipose tissue removal decreases glucose tolerance and insulin sensitivity in mice with exposure to high fat diet, Adipocyte, 4:1, 32-43, DOI: 10.4161/21623945.2014 It has been postulated that the protective effects of lower body subcutaneous adipose tissue (LBSAT) occur via its ability to sequester surplus lipid and thus serve as a "metabolic sink." However, the mechanisms that mediate this protective function are unknown thus this study addresses this postulate. Ad libitum, chow-fed mice underwent Shamsurgery or LBSAT removal (IngX, inguinal depot removal) and were subsequently provided chow (Chow; typical adipocyte expansion) or high fat diet (HFD; enhanced adipocyte expansion) for 5 weeks. Primary outcome measures included glucose tolerance and subsequent insulin response, muscle insulin sensitivity, liver and muscle triglycerides, adipose tissue gene expression, and circulating lipids and adipokines. In a follow up study the consequences of extended experiment length post-surgery (13 wks) or pre-existing glucose intolerance were examined. At 5 wks postsurgery IngX in HFD-fed mice reduced glucose tolerance and muscle insulin sensitivity and increased circulating insulin compared with HFD Sham. In Chow-fed mice, muscle insulin sensitivity was the only measurement reduced following IngX. At 13 wks circulating insulin concentration of HFD IngX mice continued to be higher than HFD Sham. Surgery did not induce changes in mice with pre-existing glucose intolerance. IngX also increased muscle, but not liver, triglyceride concentration in Chow-and HFD-fed mice 5 wks post-surgery, but chow group only at 13 wks. These data suggest that the presence of LBSAT protects against triglyceride accumulation in the muscle and HFD-induced glucose intolerance and muscle insulin resistance. These data suggest that lower body subcutaneous adipose tissue can function as a "metabolic sink."

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“…Moreover, malnutrition in elderly subjects is often caused by an inappropriate consumption of different nutrients, including proteins and micronutrients. Indeed, it has been suggested that the impairment of energy homeostasis control is one cause of malnutrition (Foster et al 2010). Paradoxically, aging has been also associated with anorexia, which results in the diminution of body weight and in cachexia (Rolland et al 2011, Biolo et al 2014.…”

Section: Introductionmentioning

confidence: 99%

Milk-soluble formula increases food intake and reduces Il6 expression in elderly rat hypothalami

Hamouda¹,

Delplanque²,

Benomar³

et al. 2015

Journal of Endocrinology

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Malnutrition in the elderly is accompanied by several metabolic dysfunctions, especially alterations in energy homeostasis regulation and a loss of insulin responsiveness. Nutritional recommendations aim to enrich food with high protein and energy supplements, and protein composition and lipid quality have been widely studied. Despite the numerous studies that have examined attempts to overcome malnutrition in the elderly through such nutritional supplementation, it is still necessary to study the effects of a combination of protein, lipids, and vitamin D (VitD). This can be done in animal models of elderly malnutrition. In the present study, we investigated the effects of several diet formulae on insulin responsiveness, inflammation, and the hypothalamic expression of key genes that are involved in energy homeostasis control. To mimic elderly malnutrition in humans, elderly Wistar rats were food restricted (R, K50%) for 12 weeks and then refed for 4 weeks with one of four different isocaloric diets: a control diet; a diet where milk soluble protein (MSP) replaced casein; a blend of milk fat, rapeseed, and DHA (MRD); or a full formula (FF) diet that combined MSP and a blend of MRD (FF). All of the refeeding diets contained VitD. We concluded that: i) food restriction led to the upregulation of insulin receptor in liver and adipose tissue accompanied by increased Tnfa in the hypothalamus; ii) in all of the refed groups, refeeding led to similar body weight gain during the refeeding period; and iii) refeeding with MSP and MRD diets induced higher food intake on the fourth week of refeeding, and this increase was associated with reduced hypothalamic interleukin 6 expression.

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Transplantation or removal of intra-abdominal adipose tissue prevents age-induced glucose insensitivity

Cited by 35 publications

References 39 publications

The Adipose Tissue Microenvironment Regulates Depot-Specific Adipogenesis in Obesity

The Adipose Tissue Microenvironment Regulates Depot-Specific Adipogenesis in Obesity

Lower body adipose tissue removal decreases glucose tolerance and insulin sensitivity in mice with exposure to high fat diet

Milk-soluble formula increases food intake and reduces Il6 expression in elderly rat hypothalami

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