Impact of micronutrient deficiencies on obesity

García, Olga P.; Long, Kurt Z.; Rosado, Jorge L.

doi:10.1111/j.1753-4887.2009.00228.x

Cited by 301 publications

(233 citation statements)

References 137 publications

(381 reference statements)

Supporting

Mentioning

222

Contrasting

Unclassified

Order By: Relevance

“…A recent meta-analysis found that prevalence of VD deficiency was 35 % higher in obese and 25 % higher in overweight compared with lean subjects (95) . In addition, 25(OH)D plasma levels are inversely correlated to all the parameters of obesity, including BMI, fat mass and waist circumference (96,97) , and increased dietary intake of VD, resulting in higher 25(OH)D plasma levels, is associated with a lower visceral adiposity (98) . The fact that adipose tissue is the main storage site for VD and/or its metabolites in the body has prompted the hypothesis that VD and/or its metabolites gets sequestered in the excess fat mass in obese persons (99) .…”

Section: Effects Of Vitamin D On Obesity and Associated Disorders Inmentioning

confidence: 99%

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

et al. 2015

View full text Add to dashboard Cite

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).

show abstract

Section: Effects Of Vitamin D On Obesity and Associated Disorders Inmentioning

confidence: 99%

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

et al. 2015

View full text Add to dashboard Cite

show abstract

“…[12][13][14] Studies in adult rodents treated with RA [15][16][17][18][19][20][21][22][23] or retinaldehyde 24 sustain an antiadiposity action of vitamin A derivatives in vivo. Furthermore, results from animal studies 16,[25][26][27][28] and human observational studies 29,30 point to an inverse relationship between vitamin A status and body fat content. The antiadiposity action of RA has been traced to increased fatty acid oxidation and energy expenditure in adipose tissues, 15,19,21,31 skeletal muscle 20,32 and the liver, 33 and to reduced peroxisome proliferator-activated receptor g (PPARg) levels and activity in white fat.…”

Section: Introductionmentioning

confidence: 99%

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

et al. 2012

View full text Add to dashboard Cite

OBJECTIVE:To assess the influence of supplementation with a moderate dose of vitamin A in early life on adipose tissue development and the response to an obesogenic diet later in life. METHODS: During the suckling period, rat pups received a daily oral dose of retinyl palmitate corresponding to three times the vitamin A ingested daily from maternal milk. Control rats received the vehicle (olive oil). Short-term effects of treatment on gene expression and morphology of white adipose tissue (WAT) were analyzed in animals on the day after weaning (day 21). To study long-term effects, control and vitamin A-treated rats were fed, after weaning, a normal fat or a high-fat (HF) diet for 16 weeks. RESULTS: WAT of vitamin A-treated young rats (day 21) was enriched in small adipocytes with a reduced expression of adipogenic markers (peroxisome proliferator-activated receptor g and lipoprotein lipase) and an increased cell proliferation potential as indicated by increased expression of proliferating cell nuclear antigen. Increased retinoic acid (RA)-induced transcriptional responses were present in the tissues of vitamin A-treated young rats (day 21) including WAT. Vitamin A-treated rats developed higher adiposity than control rats on a HF diet as indicated by body composition analysis and increased WAT depot mass, adipocyte diameter, WAT DNA content, leptinemia and adipose leptin gene expression. Excess adiposity gain in vitamin A-treated rats developed in the absence of changes in body weight and was attributable to excess adipocyte hyperplasia. No differences in adiposity were observed between vitamin A-treated rats and control rats on a normal fat diet. Total retinol levels in WAT of vitamin A-treated rats were elevated at weaning (day 21) and normalized by day 135 of age. CONCLUSION: Vitamin A intake in the early stages of postnatal life favors subsequent HF diet-induced adiposity gain through mechanisms that may relate to changes in adipose tissue development, likely mediated by RA.

show abstract

“…Higher prevalence of micronutrient deficiencies have been observed in obese individuals compared with normalweight individuals, and may be increasing the risk of fat deposition and chronic diseases (14) . Low concentrations of retinol have been found in overweight and obese individuals independent of age (15)(16)(17)(18)(19) .…”

mentioning

confidence: 99%

Effect of vitamin A deficiency on the immune response in obesity

García

2012

Proc. Nutr. Soc.

View full text Add to dashboard Cite

Obesity has been associated with low-grade systemic inflammation and with micronutrient deficiencies. Obese individuals have been found to have lower vitamin A levels and lower vitamin A intake compared with normal-weight individuals. Vitamin A plays a major role in the immune function, including innate immunity, cell-mediated immunity and humoral antibody immunity. It has also been recognised recently that vitamin A has important regulatory functions. Vitamin A status has an important effect on the chronic inflammatory response. Vitamin A deficiency increases a T-helper type 1 (Th1) response, elevates levels of proinflammatory cytokines, increases the expression of leptin, resistin and uncoupling proteins (UCP) and promotes adipogenesis. The effect of vitamin A deficiency on obesity might be increasing the risk of fat deposition and also the risk of chronic inflammation associated with obesity. Supplementation with vitamin A in vitro and in animal models has been found to reduce concentrations of adipocytokines, such as leptin and resistin. In conclusion, vitamin A deficiency increases a Th1 response in the presence of obesity and thus, increases the inflammatory process involved in chronic inflammation and fat deposition. The metabolism of leptin and other adipocytokines may play a critical role in the effect of vitamin A deficiency in the inflammatory response observed in obesity.

show abstract

Impact of micronutrient deficiencies on obesity

Cited by 301 publications

References 137 publications

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

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

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

Effect of vitamin A deficiency on the immune response in obesity

Contact Info

Product

Resources

About