Mitochondriogenesis and apoptosis: possible cause of vitamin A-mediated adipose loss in WNIN/Ob-obese rats

Denne nevner at kronisk tilskudd av Vitamin A på 53mg/kg øker produksjon av mitokondrier og derigjennom bidrar til vektnedgang. Denne dosen blir 5300mg for en på 100kg. Studien nevner også at A vitamin aktiverer «uncouling protein» (UCP1) i mitokondriene som bidrar til termogenese (produksjon av varme i cellen). Det betyr at metabolismen øker men uten at man produserer mer frie radikaler.


Previously, we reported that vitamin A-enriched diet (129 mg/kg diet) intake reduces the adiposity development in obese rats of WNIN/Ob strain. Here, we hypothesize that dose lesser than 129 mg of vitamin A/kg diet would also be effective in ameliorating the development of obesity in these rats.


Five-month-old male lean and obese rats designated as A & B were divided into four subgroups (I, II, III and IV) consisting of 8 rats from each phenotype and received diets containing 2.6 mg (control group), 26 mg, 52 mg and 129 mg vitamin A/kg diet as retinyl palmitate for 20 weeks. Body composition and morphological analysis of brown adipose tissue (BAT) was analyzed. Expression of uncoupling protein 1 (UCP1), retinoic acid receptor α (RARα) and retinoid X receptor α (RXRα) in BAT and levels of Bcl2 and Bax in epididymal white adipose tissue (eWAT) were determined by immunoblotting.


Vitamin A supplementation to obese rats at doses of 52 and 129 mg/kg diet showed reduced body weight gain and adiposity compared to control diet-fed obese rats receiving 2.6 mg of vitamin A/kg diet. In BAT of obese rats, vitamin A supplementation at doses of 26 and 52 mg of vitamin A/kg diet resulted in increased UCP1 expression with concomitant decrease in RARα and RXRα levels compared to control diet-fed obese rats. Further, transmission electron microscopy study revealed an increase in number of BAT mitochondria of obese rats supplemented with 26 and 52 mg of vitamin A/kg diet. Also, obese rats fed on 52 mg/kg diet resulted in increased apoptosis by altering the ratio of Bcl2 to Bax protein levels in eWAT. Notably, most of these changes were not observed in lean rats fed vitamin A-enriched diets.


In conclusion, chronic consumption of 52 mg of vitamin A/kg diet seems to be an effective dose in ameliorating obesity possibly through mitochondriogenesis, UCP1-mediated thermogenesis in BAT and apoptosis in eWAT of obese rats. Therefore, the role of dietary vitamin A in correcting human obesity would be of unquestionable relevance and can only be addressed by future studies.

The effect of vitamin A supplementation on thyroid function in premenopausal women.

Tyroid problemer er svært vanlig. Det gir trøtthet, depresjon, lav energi, og et hav av medfølgende plager. En viktig del av øke tyroidea ar å få nok A-vitamin. Her er en studie som nevner at 25000 IU A-vitamin (7500mg) gir en signifikant reduksjon i TSH (som hemmer tyroidea).


Vitamin A and its retinoid derivates play an important role in regulation of normal growth and development. Vitamin A has been shown to regulate thyroid hormone metabolism and inhibit thyroid-stimulating hormone (TSH) secretion via down regulation of TSH-β gene expression; however, the effect of vitamin A on thyroid function in obese individuals who are at higher risk of subclinical hypothyroidism is still unclear. In the present study we investigate the impact of vitamin A supplementation on thyroid function in obese women.


A 4-month randomized, double blind controlled trial was conducted among 84 healthy women aged 17-50 years old: 56 were obese (body mass index [BMI] 30-35 kg/m(2)) and 28 were nonobese (BMI 18.5-24.9 kg/m(2)). Obese women were randomly allocated to receive either vitamin A (25,000 IU/d retinyl palmitate) or placebo. Nonobese women received vitamin A. At baseline and 4 months after intervention, serum concentrations of TSH, total thyroxine (T4), total triiodothyronine (T3), retinol-binding protein (RBP), and transthyretin (TTR) were measured.


Baseline concentrations of thyroid hormones, RBP and TTR were not significantly different between groups. Vitamin A caused a significant reduction in serum TSH concentrations in obese (p = 0.004) and nonobese (p = 0.001) groups. Serum T3 concentrations also increased in both obese and nonobese vitamin A-treated groups (p < 0.001). Serum T4 decreased in all 3 groups after treatment. The results showed a significant reduction in serum RBP in the obese group after vitamin A supplementation (p = 0.007), but no significant change was seen in serum TTR.


Serum TSH concentrations in vitamin A-treated subjects were significantly reduced; therefore, vitamin A supplementation might reduce the risk of subclinical hypothyroidism in premenopausal women.