It's Not How Fat You Are, It's What You Do with It That Counts

Virtue, Samuel; Vidal-Puig, António

doi:10.1371/journal.pbio.0060237

Cited by 260 publications

(191 citation statements)

References 33 publications

(39 reference statements)

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“…This improvement of metabolic flexibility correlated with changes in body weight, adiposity and glycaemic control in accordance with the notion that metabolic flexibility is closely associated with insulin sensitivity [2,32] and that impaired flexibility represents an early defect in the development of type 2 diabetes [35]. Metabolic syndrome is linked to inflammatory changes in both WAT and liver [1]. In this study, in accordance with the previous findings [17,18,21], dietary LC n-3 PUFA supplementation resulted in the inhibition of formation of various LC n-6 PUFA-derived pro-inflammatory eicosanoids in both tissues as well as in the induction of the antiinflammatory molecules.…”

Section: Discussionsupporting

confidence: 84%

“…When (post)prandial plasma levels of NEFA and triacylglycerol (TG) exceed the storage capacity of WAT [1], other tissues including the liver and muscle become overloaded with lipids, which results in insulin resistance, the key event in the pathophysiology of metabolic syndrome [2]. The important role of WAT in energy homeostasis is underscored by the findings that WAT is one of the key organs affected by calorie restriction, the most effective strategy to prolong a healthy life in several species [3], and by the fact that accumulation of body fat can be reduced through upregulation of lipid catabolism in WAT [4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

“…Importantly, LC n-3 PUFA also decrease inflammation [14], including obesity-associated low-grade inflammation of WAT [15,16], characterised by altered secretion patterns of adipokines, which contributes to insulin resistance [1]. The anti-inflammatory effects of LC n-3 PUFA probably depend on the formation of their active metabolites.…”

Section: Introductionmentioning

confidence: 99%

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Synergistic induction of lipid catabolism and anti-inflammatory lipids in white fat of dietary obese mice in response to calorie restriction and n-3 fatty acids

et al. 2011

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Aims/hypothesis Calorie restriction is an essential component in the treatment of obesity and associated diseases. Longchain n-3 polyunsaturated fatty acids (LC n-3 PUFA) act as natural hypolipidaemics, reduce the risk of cardiovascular disease and could prevent the development of obesity and insulin resistance. We aimed to characterise the effectiveness and underlying mechanisms of the combination treatment with LC n-3 PUFA and 10% calorie restriction in the prevention of obesity and associated disorders in mice. Methods Male mice (C57BL/6J) were habituated to a cornoil-based high-fat diet (cHF) for 2 weeks and then randomly assigned to various dietary treatments for 5 weeks or 15 weeks: (1) cHF, ad libitum; (2) cHF with LC n-3 PUFA concentrate replacing 15% (wt/wt) of dietary lipids (cHF+F), ad libitum; (3) cHF with calorie restriction (CR; cHF+CR); and (4) cHF+F+CR. Mice fed a chow diet were also studied. Results We show that white adipose tissue plays an active role in the amelioration of obesity and the improvement of glucose homeostasis by combining LC n-3 PUFA intake and calorie restriction in cHF-fed mice. Specifically in the epididymal fat in the abdomen, but not in other fat depots, synergistic induction of mitochondrial oxidative capacity and lipid catabolism was observed, resulting in increased oxidation of metabolic fuels in the absence of mitochondrial uncoupling, while low-grade inflammation was suppressed, reflecting changes in tissue levels of anti-inflammatory lipid mediators, namely 15-deoxy-Δ 12,15 -prostaglandin J 2 and protectin D1. Conclusions/interpretation White adipose tissue metabolism linked to its inflammatory status in obesity could be modulated by combination treatment using calorie restriction and dietary LC n-3 PUFA to improve therapeutic strategies for metabolic syndrome.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

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Synergistic induction of lipid catabolism and anti-inflammatory lipids in white fat of dietary obese mice in response to calorie restriction and n-3 fatty acids

et al. 2011

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“…In addition, components of the TNFα and IL-1-β-signalling pathways prevent PPARγ binding to DNA by associating with NF-κB (72) . This (53) . The hypothesis proposes that in positive energy balance, subcutaneous adipose tissue (SAT) has a limited capacity to increase its mass.…”

Section: Adipogenesismentioning

confidence: 87%

Adipose tissue dysregulation and metabolic consequences in childhood and adolescent obesity: potential impact of dietary fat quality

et al. 2014

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Evidence suggests that at a population level, childhood and adolescent obesity increase the long-term risk of chronic diseases such as type 2 diabetes and CVD. At an individual level, however, the metabolic consequences of obesity in youth vary immensely. Despite comparable BMI, some adolescents develop impaired glucose tolerance while others maintain normal glucose homeostasis. It has been proposed that the variation in the capacity to store lipid in the subcutaneous adipose tissue (SAT) may partially discriminate metabolically healthy from unhealthy obesity. In positive energy balance, a decreased capacity to expand SAT may drive lipid accumulation to visceral adipose tissue, liver and skeletal muscle. This state of lipotoxicity is associated with chronic low-grade inflammation, insulin resistance and dyslipidaemia. The present review examines the differential adipose tissue development and function in children and adolescents who exhibit metabolic dysregulation compared with those who are protected. Additionally, the role of manipulating dietary fat quality to potentially prevent and treat metabolic dysfunction in obesity will be discussed. The findings of the present review highlight the need for further randomised controlled trials to establish the effect of dietary n-3 PUFA on the metabolic phenotype of obese children and adolescents. Furthermore, using a personalised nutrition approach to target interventions to those at risk of, or those with established metabolic dysregulation may optimise the efficacy of modifying dietary fat quality.

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“…15 It was suggested that adipose tissue expandability is a more important determinant of obesity-associated metabolic disorders than the absolute amount of adipose tissue an individual possesses. 16 Moreover, larger fat cells are associated with a low-grade adipose tissue inflammation, another key factor linking obesity with insulin resistance. 13,14,[17][18][19] Enhanced secretion of chemoattractants in obese state, like monocyte chemoattractant protein-1 (MCP-1), is believed to promote migration of macrophages 20,21 as well as other immune cells 22 into the tissue accompanied by the phenotypic switch of macrophages to proinflammatory state.…”

Section: Introductionmentioning

confidence: 99%

Sex differences during the course of diet-induced obesity in mice: adipose tissue expandability and glycemic control

et al. 2011

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Objective: Adverse effects of obesity on glucose homeostasis are linked to low-grade adipose tissue inflammation and accumulation of lipids in non-adipose tissues. The goal of this study was to evaluate the role of adipose tissue plasticity in a less severe deterioration of glucose homeostasis in females compared with males during the course of high-fat (HF) feeding in mice. Design: Mice of the C57BL/6N strain were fed either a chow or obesogenic HF diet for up to 35 weeks after weaning. Metabolic markers and hormones in plasma, glucose homeostasis, adipocyte size and inflammatory status of gonadal (gWAT) and subcutaneous (scWAT) adipose depots and liver steatosis were evaluated at 15 and 35 weeks of HF feeding. Results: HF-fed males were heavier than females until week B20, after which the body weights stabilized at a similar level (55-58 g) in both sexes. Greater weight gain and fat accumulation in females were associated with larger adipocytes in gWAT and scWAT at week 35. Although adipose tissue macrophage infiltration was in general less frequent in scWAT, it was reduced in both fat depots of female as compared with male mice; however, the expression of inflammatory markers in gWAT was similar in both sexes at week 35. In females, later onset of the impairment of glucose homeostasis and better insulin sensitivity were associated with higher plasma levels of adiponectin (weeks 0, 15 and 35) and reduced hepatosteatosis (weeks 15 and 35). Conclusions: Compared with males, female mice demonstrate increased capacity for adipocyte enlargement in response to a long-term HF feeding, which is associated with reduced adipose tissue macrophage infiltration and lower fat deposition in the liver, and with better insulin sensitivity. Our data suggest that adipose tissue expandability linked to adiponectin secretion might have a role in the sex differences observed in obesity-associated metabolic disorders.

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It's Not How Fat You Are, It's What You Do with It That Counts

Cited by 260 publications

References 33 publications

Synergistic induction of lipid catabolism and anti-inflammatory lipids in white fat of dietary obese mice in response to calorie restriction and n-3 fatty acids

Synergistic induction of lipid catabolism and anti-inflammatory lipids in white fat of dietary obese mice in response to calorie restriction and n-3 fatty acids

Adipose tissue dysregulation and metabolic consequences in childhood and adolescent obesity: potential impact of dietary fat quality

Sex differences during the course of diet-induced obesity in mice: adipose tissue expandability and glycemic control

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