Regulation of fructose 2,6‐bisphosphate levels in cold‐acclimated brown adipose tissue of rat

Sobrino, Francisco; Gualberto, Antonio; Pintado, Elizabeth

doi:10.1016/0014-5793(88)80804-4

Cited by 3 publications

(3 citation statements)

References 19 publications

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“…Other Enzymatic Assays. Lactate dehydrogenase (LDH) and pyruvate kinase (PK) were measured by standard procedures in the 12,000 g supernatant of Jurkat T cell homogenate as described previously (22). Hexokinase (HK) was measured in the homogenate of Jurkat T cells as reported elsewhere (23).…”

Section: Methodsmentioning

confidence: 99%

Methylation-Dependent Gene Silencing Induced by Interleukin 1β via Nitric Oxide Production

Hmadcha

Bedoya

Sobrino

et al. 1999

The Journal of Experimental Medicine

196

134

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Interleukin (IL)-1β is a pleiotropic cytokine implicated in a variety of activities, including damage of insulin-producing cells, brain injury, or neuromodulatory responses. Many of these effects are mediated by nitric oxide (NO) produced by the induction of NO synthase (iNOS) expression. We report here that IL-1β provokes a marked repression of genes, such as fragile X mental retardation 1 (FMR1) and hypoxanthine phosphoribosyltransferase (HPRT), having a CpG island in their promoter region. This effect can be fully prevented by iNOS inhibitors and is dependent on DNA methylation. NO donors also cause FMR1 and HPRT gene silencing. NO-induced methylation of FMR1 CpG island can be reverted by demethylating agents which, in turn, produce the recovery of gene expression. The effects of IL-1β and NO appear to be exerted through activation of DNA methyltransferase (DNA MeTase). Although exposure of the cells to NO does not increase DNA MeTase gene expression, the activity of the enzyme selectively increases when NO is applied directly on a nuclear protein extract. These findings reveal a previously unknown effect of IL-1β and NO on gene expression, and demonstrate a novel pathway for gene silencing based on activation of DNA MeTase by NO and acute modification of CpG island methylation.

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Section: Methodsmentioning

confidence: 99%

Methylation-Dependent Gene Silencing Induced by Interleukin 1β via Nitric Oxide Production

Hmadcha

Bedoya

Sobrino

et al. 1999

The Journal of Experimental Medicine

196

134

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“…Methionine sulfoxide, fructose 2,6-bisphosphate (Sobrino et al, 1988), cyclic guanosine monophosphate (cGMP) (Hoffmann et al, 2015), and pantothenic acid (vitamin B5) levels in serum were significantly higher in control mice at both 22 C and 4 C compared to ABX individuals. In contrast, 11b-prostaglandin F2awas significantly lower in control mice at both 22 C and 4 C. A previous study reported that the gut microbiota may regulate tryptophan metabolism through tryptophan hydroxylase and promote serotonin biosynthesis (Yano et al, 2015).…”

Section: Gut Microbiota Depletion Damages Thermoregulationmentioning

confidence: 99%

Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue

et al. 2019

Cell Reports

211

160

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Graphical AbstractHighlights d Mice lacking gut microbiota have impaired UCP1-dependent thermogenesis in cold d These effects are replicated in germ-free mice treated with CL-316243 d IL-4 has no differential effect on energy metabolism in either control or ABX mice d Gavage of ABX mice with butyrate partially rescues the effects on BAT recruitment SUMMARYThe relation between gut microbiota and the host has been suggested to benefit metabolic homeostasis. Brown adipose tissue (BAT) and beige adipocytes facilitate thermogenesis to maintain host core body temperature during cold exposure. However, the potential impact of gut microbiota on the thermogenic process is confused. Here, we evaluated how BAT and white adipose tissue (WAT) responded to temperature challenges in mice lacking gut microbiota. We found that microbiota depletion via treatment with different cocktails of antibiotics (ABX) or in germfree (GF) mice impaired the thermogenic capacity of BAT by blunting the increase in the expression of uncoupling protein 1 (UCP1) and reducing the browning process of WAT. Gavage of the bacterial metabolite butyrate increased the thermogenic capacity of ABX-treated mice, reversing the deficit. Our results indicate that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated via butyrate.

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“…There are several isoforms of PK, including two muscle isoforms: muscle pyruvate kinase 1 and 2 ( Pkm1 and Pkm2 ). Studies with rodents have demonstrated a cold-induced increase in activity of HK, PFK and PK in BAT 9–11 . Consistent with this, we have reported increased expression of many glycolytic enzymes in BAT from cold-exposed mice 8 .…”

Section: Introductionmentioning

confidence: 99%

Regulation of glycolysis in brown adipocytes by HIF-1α

Basse

Isidor

Winther

et al. 2017

Sci Rep

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Brown adipose tissue takes up large amounts of glucose during cold exposure in mice and humans. Here we report an induction of glucose transporter 1 expression and increased expression of several glycolytic enzymes in brown adipose tissue from cold-exposed mice. Accordingly, these genes were also induced after β-adrenergic activation of cultured brown adipocytes, concomitant with accumulation of hypoxia inducible factor-1α (HIF-1α) protein levels. HIF-1α accumulation was dependent on uncoupling protein 1 and generation of mitochondrial reactive oxygen species. Expression of key glycolytic enzymes was reduced after knockdown of HIF-1α in mature brown adipocytes. Glucose consumption, lactate export and glycolytic capacity were reduced in brown adipocytes depleted of Hif-1α. Finally, we observed a decreased β-adrenergically induced oxygen consumption in Hif-1α knockdown adipocytes cultured in medium with glucose as the only exogenously added fuel. These data suggest that HIF-1α-dependent regulation of glycolysis is necessary for maximum glucose metabolism in brown adipocytes.

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Regulation of fructose 2,6‐bisphosphate levels in cold‐acclimated brown adipose tissue of rat

Cited by 3 publications

References 19 publications

Methylation-Dependent Gene Silencing Induced by Interleukin 1β via Nitric Oxide Production

Methylation-Dependent Gene Silencing Induced by Interleukin 1β via Nitric Oxide Production

Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue

Regulation of glycolysis in brown adipocytes by HIF-1α

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