Vitamin D protects against diet-induced obesity by enhancing fatty acid oxidation

Marcotorchino, Julie; Tourniaire, Franck; Astier, Julien; Karkeni, Esma; Canault, Matthias; Amiot, Marie-Josèphe; Bendahan, David; Bernard, Monique; Martin, Jean-Charles; Giannesini, Benoı̂t; Landrier, Jean‐François

doi:10.1016/j.jnutbio.2014.05.010

Cited by 119 publications

(114 citation statements)

References 42 publications

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“…In addition, we recently demonstrated that VD supplementation of high-fat diet reduced the expression of proinflammatory cytokines and chemokines and inhibited macrophage infiltration in the adipose tissue of obese mice (80) . Similar effects of VD supplementation were found in an acute inflammation model (intraperitoneal injection of LPS) where no modification of body weight was measured (80) , which strongly suggests that the decreased inflammatory status of adipose tissue observed in obese mice is not only a consequence of reduced fat mass (69) but is also driven by an anti-inflammatory effect of VD per se.…”

Section: Regulation Of Inflammationsupporting

confidence: 65%

Vitamin D modulates adipose tissue biology: possible consequences for obesity?

et al. 2015

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Cross-sectional studies depict an inverse relationship between vitamin D (VD) status reflected by plasma 25-hydroxy-vitamin D and obesity. Furthermore, recent studies in vitro and in animal models tend to demonstrate an impact of VD and VD receptor on adipose tissue and adipocyte biology, pointing to at least a part-causal role of VD insufficiency in obesity and associated physiopathological disorders such as adipose tissue inflammation and subsequent insulin resistance. However, clinical and genetic studies are far less convincing, with highly contrasted results ruling out solid conclusions for the moment. Nevertheless, prospective studies provide interesting data supporting the hypothesis of a preventive role of VD in onset of obesity. The aim of this review is to summarise the available data on relationships between VD, adipose tissue/adipocyte physiology, and obesity in order to reveal the next key points that need to be addressed before we can gain deeper insight into the controversial VD-obesity relationship.Adipose tissue: Vitamin D: Obesity: Inflammation: Adipocytes: Nutrients: Nutrition Vitamin D: a brief overview Vitamin D (VD; calciferol) is a hormone mainly described for its role as a regulator of phosphate and calcium homeostasis (1) . It can be obtained through animal (VD 3 , cholecalciferol) or plant (VD 2 , ergocalciferol) food sources. Only a few foodstuffs contain significant amounts of VD, the main sources being fish liver oils, fatty fish (sardines, herring and mackerel) and egg yolk (2,3) , but small quantities are also found in fortified milk, orange juice, bread and cereals. Alternatively, VD 3 is produced endogenously in the skin after UVB irradiation from the precursor 7-dehydrocholesterol to give pre-VD 3 , which is further isomerised to VD 3 before being released into the circulation (4) . Classical estimates have assigned a majority (70-90 %) of VD supply to dermal synthesis, but a recent paper revised this figure down to just 10-25 % of VD supply (5) and posited that dietary intake of 25-hydroxy-vitamin D (25(OH)D) is a significant contributor to total VD input.Adipose tissue is a major storage site for vitamin D Despite limited data, it is widely accepted that adipose tissue is a reservoir for VD in human subjects and rats (6)(7)(8)(9)(10) . Interestingly, visceral fat was found to contain 20 % more VD than subcutaneous fat (11) . Heaney et al. (12) calculated that 65 % of total VD in the body is in the form of D 3 , for which adipose tissue and skeletal muscle appear to be the main body stores (accounting for 73 and 16 %, respectively).

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Section: Regulation Of Inflammationsupporting

confidence: 65%

Vitamin D modulates adipose tissue biology: possible consequences for obesity?

et al. 2015

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“…IU/kg). 13 This contrary result could be explained by a differing capacity of female mice 13 to respond to dietary vitamin D (as compared to the results obtained using male mice described above 11,12 In other studies, we observed no significant effect of lower doses of dietary vitamin [33][34][35] with the VDR -/-mice also exhibiting reduced fasting glucose and insulin levels. 33 The VDR may also be important for mediating the progression of non-alcoholic fatty liver disease (NAFLD) and insulin resistance as reduced hepatic steatosis and triglyceride levels were observed in apoE -/-VDR -/-mice fed a high fat diet.…”

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confidence: 87%

Ultraviolet radiation, vitamin D and the development of obesity, metabolic syndrome and type-2 diabetes

Gorman

Lucas

Allen-Hall

et al. 2017

Photochem Photobiol Sci

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“…Similarly, a recent study reported that VD deficiency exacerbates tenofovirinduced elevation of serum levels of TC and TG in rats (Canale et al, 2014). Moreover, it has been reported that VD deficiency in obese rats exacerbated nonalcoholic fatty liver disease and increased serum TG level (Roth et al, 2012), whereas VD supplementation successfully protected against high-fat diet-induced obesity and hepatic steatosis, which paralleled with improvement of glucose homeostasis and serum lipid profile (Marcotorchino et al, 2014;Yin et al, 2012). Though antipsychotic medication-emergent weight gain is the most commonly reported side effect in humans and is strongly associated with increased appetite, the results from animal studies are conflicting (Boyda et al, 2010;Kluge et al, 2007).…”

Section: Discussionmentioning

confidence: 80%