Enhanced pan‐peroxisome proliferator‐activated receptor gene and protein expression in adipose tissue of diet‐induced obese mice treated with telmisartan

Penna-de-Carvalho, Aline; Graus-Nunes, Francielle; Rabelo-Andrade, Júlia; Mandarim-de-Lacerda, Carlos Alberto; Souza-Mello, Vanessa

doi:10.1113/expphysiol.2014.081596

Cited by 24 publications

(18 citation statements)

References 61 publications

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“…A high-fish-oil diet (with 45% of total energy content from fish oil) decreased blood glucose in lipopolysaccharide-induced inflammation in mice [11], and a high amount of n-3 PUFAs improved the glycemic curve in rats [1]. Feeding mice an obesogenic diet leads to impaired insulin signaling in adipose tissue, with a reduction of AKT phosphorylation [27], as we saw in our HF-L group. On the contrary, fish oil appears to improve AKT phosphorylation, enhancing insulin signaling [28].…”

Section: Discussionmentioning

confidence: 56%

A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice

Bargut

Mandarim-de-Lacerda

Águila

2015

The Journal of Nutritional Biochemistry

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Section: Discussionmentioning

confidence: 56%

A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice

Bargut

Mandarim-de-Lacerda

Águila

2015

The Journal of Nutritional Biochemistry

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“…Recent studies have linked the use of fenofibrate (PPAR‐α agonist) with reduced body mass (BM), although the mechanisms remained to be elucidated . Recently, the activation of PPAR‐α and PPAR‐γ isoforms by telmisartan triggered high UCP‐1 gene and protein expression, leading to increased thermogenesis and EE …”

Section: Introductionmentioning

confidence: 99%

PPAR‐α agonist elicits metabolically active brown adipocytes and weight loss in diet‐induced obese mice

Rachid

Penna-de-Carvalho

Bringhenti

et al. 2015

Cell Biochemistry & Function

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Obesity is considered a public health problem worldwide. Fenofibrate, a selective peroxisome proliferator-activated receptor α (PPAR-α) agonist, elicits weight loss in animal models. This study aimed to examine the effects of fenofibrate on energy expenditure, body mass (BM) and gene expression of thermogenic factors in brown adipose tissue of diet-induced obese mice. Male C57BL/6 mice were fed a standard chow (SC; 10% lipids) diet or a high-fat (HF; 50% lipids) diet for 10 weeks. Afterwards, groups were subdivided as SC, SC-F, HF and HF-F (n = 10, each). Treatment with fenofibrate (100 mg kg(-1) BM mixed into the diet) lasted 5 weeks. Treated groups had reduced final BM compared with their counterparts (p < 0·05), explained by the increase in energy expenditure, CO2 production and O2 consumption after treatment with fenofibrate (p < 0·05). Similarly, genes involved in thermogenesis as PPAR-α, PPAR-γ coactivator 1α, nuclear respiratory factor 1, mitochondrial transcription factor A (Tfam), PR domain containing 16 (PRDM16), β-3 adrenergic receptor (β3-AR), bone morphogenetic protein 8B and uncoupling protein 1 were significantly expressed in brown adipocytes after the treatment (p < 0·05). All observations ensure that selective PPAR-α agonist can induce thermogenesis by increasing energy expenditure and enhancing the expression of genes involved in the thermogenic pathway. These results suggest fenofibrate as a coadjutant drug for the treatment of obesity.

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“…It can be argued that full activation of PPAR-gamma favors the transcription of lipogenic transcription factors, such as SREBP-1c, and even though animals benefit from antiinflammatory effects of high adiponectin levels, the upregulation of lipogenesis NAFLD, highlighting the importance of PPAR activation to treat NAFLD. Telmisartan also yields decreased expression of Nuclear factor kB target genes, such as TNF-alpha and interleukin-6 in diet-induced obese mice, which coupled with increased adiponectin prevent these animals from NASH onset [21,67] . In resemblance with telmisartan, ragaglitazar, a dual PPAR-alpha/PPAR-gamma agonist, tackled hepatic insulin resistance, hepatic steatosis and overweight in a mouse model of metabolic syndrome, whereas total PPAR-gamma agonist rosiglitazone elicited visceral adiposity and hepatomegaly [68] .…”

Section: Targeting Ppars To Treat Nafldmentioning

confidence: 99%

Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

Souza-Mello¹

2015

WJH

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152

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and microsomal omega-oxidation, being markedly decreased by high-fat (HF) intake. PPAR-beta/delta is crucial to the regulation of forkhead box-containing protein O subfamily-1 expression and, hence, the modulation of enzymes that trigger hepatic gluconeogenesis. In addition, PPAR-beta/delta can activate hepatic stellate cells aiming to the hepatic recovery from chronic insult. On the contrary, PPAR-gamma upregulation by HF diets maximizes NAFLD through the induction of lipogenic factors, which are implicated in the fatty acid synthesis. Excessive dietary sugars also upregulate PPAR-gamma, triggering de novo lipogenesis and the consequent lipid droplets deposition within hepatocytes. Targeting PPARs to treat NAFLD seems a fruitful approach as PPAR-alpha agonist elicits expressive decrease in hepatic steatosis by increasing mitochondrial beta-oxidation, besides reduced lipogenesis. PPAR-beta/delta ameliorates hepatic insulin resistance by decreasing hepatic gluconeogenesis at postprandial stage. Total PPAR-gamma activation can exert noxious effects by stimulating hepatic lipogenesis. However, partial PPAR-gamma activation leads to benefits, mainly mediated by increased adiponectin expression and decreased insulin resistance. Further studies are necessary aiming at translational approaches useful to treat NAFLD in humans worldwide by targeting PPARs. AbstractLately, the world has faced tremendous progress in the understanding of non-alcoholic fatty liver disease (NAFLD) pathogenesis due to rising obesity rates. Peroxisome proliferator-activated receptors (PPARs) are transcription factors that modulate the expression of genes involved in lipid metabolism, energy homeostasis and inflammation, being altered in diet-induced obesity. Experimental evidences show that PPAR-alpha is the master regulator of hepatic beta-oxidation (mitochondrial and peroxisomal)

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Enhanced pan‐peroxisome proliferator‐activated receptor gene and protein expression in adipose tissue of diet‐induced obese mice treated with telmisartan

Cited by 24 publications

References 61 publications

A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice

A high-fish-oil diet prevents adiposity and modulates white adipose tissue inflammation pathways in mice

PPAR‐α agonist elicits metabolically active brown adipocytes and weight loss in diet‐induced obese mice

Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

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