Vitamin A supplementation induces adipose tissue loss through apoptosis in lean but not in obese rats of the WNIN/Ob strain

Jeyakumar, Shanmugam M.; Vajreswari, Ayyalasomayajula; Sesikeran, B.; Giridharan, Nappan Veettil

doi:10.1677/jme.1.01838

Cited by 34 publications

(33 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In contrast, clinical trials have reported that increasing the intake of calcium‐rich foods in isocaloric diets reduces adiposity, 128,134 which suggests that a pre‐existing calcium deficiency increases the risk of obesity. The finding that retinoic acid, when given as a supplement or injected into mice, reduces adiposity similarly suggests that pre‐existing vitamin A status may also be a determinant of obesity 37–39 …”

Section: Resultsmentioning

confidence: 99%

“…Animal studies have shown that retinoic acid (RA) reduces body weight, body fat content, and adipocyte size when injected into mice in the form of all‐trans retinoic acid (atRA) 34–36 . Similarly, obese rats supplemented for 2 months with high doses of vitamin A demonstrated significant decreases in body weight gain, adiposity index, and retroperitoneal white adipose tissue compared to lean rats 37–39 . Retinaldheyde, a metabolite derived from RA, also reduces fat and increases insulin sensitivity in obese mice 40 …”

Section: Effect Of Vitamin a Deficiency On Obesitymentioning

confidence: 99%

See 1 more Smart Citation

Impact of micronutrient deficiencies on obesity

2009

View full text Add to dashboard Cite

Micronutrient deficiencies have been found in obese individuals across age groups worldwide. While the effects of micronutrient deficiencies on human functions have been studied widely in different populations, there is limited information on how these micronutrient deficiencies affect obese populations. An examination of the available literature suggests associations exist between micronutrient deficiencies and obesity in different populations. These associations and possible mechanisms of the deficiencies' metabolic effects, such as their influence on leptin and insulin metabolism, are discussed here. Further studies are needed to clarify the roles of the different micronutrient deficiencies with respect to obesity and its comorbid conditions.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Effect Of Vitamin a Deficiency On Obesitymentioning

confidence: 99%

Impact of micronutrient deficiencies on obesity

2009

View full text Add to dashboard Cite

show abstract

“…High dietary retinol intake has been reported by Jeyakumar et al to decrease body weight and WAT mass in both lean and obese rats (37,38) but other investigations involving mice showed no change in body weight and WAT mass upon high dietary retinol intake for 18 weeks (39). These differences may arise due to differences in the species studied.…”

Section: Retinoid Regulation Of Adipocyte Biologymentioning

confidence: 96%

Retinoids: Potent regulators of metabolism

Brun¹,

Yang²,

Lee³

et al. 2012

BioFactors

View full text Add to dashboard Cite

Retinoids (vitamin A and its analogs) are highly potent regulators of cell differentiation, cell proliferation, and apoptosis. Because of these activities, retinoids have been most extensively studied in the contexts of embryonic development and of proliferative diseases, especially cancer and skin disease. Recently, there has been considerable new research interest focused on gaining understanding of the roles that retinoids and/or retinoid-related proteins may have in the development of metabolic diseases, primarily obesity, diabetes, and dyslipidemia. This review will summarize recent advances that have been made in these areas, focusing on the role of retinoids in modulating adipogenesis, the roles of retinoids and retinoid-related proteins as signaling molecules linking obesity with the development of type II diabetes, the roles of retinoids in pancreatic β-cell biology/insulin secretion, and the actions of retinoids in hepatic steatosis.

show abstract

“…Vitamin A-enriched diet has been shown to decrease adiposity and alter adipose tissue gene expression in rats [9]. Our previous studies on supplementation of high but non-toxic dose of vitamin A to obese rats of WNIN/Ob strain have shown to decrease adiposity [10,11]. So far, no studies have addressed the role of vitamin A in the regulation of 11β-HSD1 activity in normal and obese conditions.…”

Section: Introductionmentioning

confidence: 99%

Vitamin A decreases pre-receptor amplification of glucocorticoids in obesity: study on the effect of vitamin A on 11beta-hydroxysteroid dehydrogenase type 1 activity in liver and visceral fat of WNIN/Ob obese rats

Sakamuri

Ananthathmakula

Veettil

et al. 2011

Nutr J

View full text Add to dashboard Cite

Background11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes the conversion of inactive glucocorticoids to active glucocorticoids and its inhibition ameliorates obesity and metabolic syndrome. So far, no studies have reported the effect of dietary vitamin A on 11β-HSD1 activity in visceral fat and liver under normal and obese conditions. Here, we studied the effect of chronic feeding of vitamin A-enriched diet (129 mg/kg diet) on 11β-HSD1 activity in liver and visceral fat of WNIN/Ob lean and obese rats.MethodsMale, 5-month-old, lean and obese rats of WNIN/Ob strain (n = 16 for each phenotype) were divided into two subgroups consisting of 8 rats of each phenotype. Control groups received stock diet containing 2.6 mg vitamin A/kg diet, where as experimental groups received diet containing 129 mg vitamin A/Kg diet for 20 weeks. Food and water were provided ad libitum. At the end of the experiment, tissues were collected and 11β-HSD1 activity was assayed in liver and visceral fat.ResultsVitamin A supplementation significantly decreased body weight, visceral fat mass and 11β-HSD1 activity in visceral fat of WNIN/Ob obese rats. Hepatic 11β-HSD1 activity and gene expression were significantly reduced by vitamin A supplementation in both the phenotypes. CCAAT/enhancer binding protein α (C/EBPα), the main transcription factor essential for the expression of 11β-HSD1, decreased in liver of vitamin A fed-obese rats, but not in lean rats. Liver × receptor α (LXRα), a nuclear transcription factor which is known to downregulate 11β-HSD1 gene expression was significantly increased by vitamin A supplementation in both the phenotypes.ConclusionsThis study suggests that chronic consumption of vitamin A-enriched diet decreases 11β-HSD1 activity in liver and visceral fat of WNIN/Ob obese rats. Decreased 11β-HSD1 activity by vitamin A may result in decreased levels of active glucocorticoids in adipose tissue and possibly contribute to visceral fat loss in these obese rats. Studying the role of various nutrients on the regulation of 11β-HSD1 activity and expression will help in the evolving of dietary approaches to treat obesity and insulin resistance.

show abstract

Vitamin A supplementation induces adipose tissue loss through apoptosis in lean but not in obese rats of the WNIN/Ob strain

Cited by 34 publications

References 43 publications

Impact of micronutrient deficiencies on obesity

Impact of micronutrient deficiencies on obesity

Retinoids: Potent regulators of metabolism

Vitamin A decreases pre-receptor amplification of glucocorticoids in obesity: study on the effect of vitamin A on 11beta-hydroxysteroid dehydrogenase type 1 activity in liver and visceral fat of WNIN/Ob obese rats

Contact Info

Product

Resources

About