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Chronic exercise reduces hypothalamic transforming growth factor-β1 in middle-aged obese mice.

ABSTRACT: Obesity and aging are associated with hypothalamic inflammation, hyperphagia and abnormalities in the thermogenesis control. It has been demonstrated that the association between aging and obesity induces hypothalamic inflammation and metabolic disorders, at least in part, through the atypical hypothalamic transforming growth factor-β (TGF-β1). Physical exercise has been used to modulate several metabolic parameters. Thus, the aim of this study was to evaluate the impact of chronic exercise on TGF-β1 expression in the hypothalamus of Middle-Aged mice submitted to a one year of high-fat diet (HFD) treatment. We observed that long-term of HFD-feeding induced hypothalamic TGF-β1 accumulation, potentiated the hypothalamic inflammation, body weight gain and defective thermogenesis of Middle-Aged mice when compared to Middle-Aged animals fed on chow diet. As expected, chronic exercise induced negative energy balance, reduced food consumption and increasing the energy expenditure, which promotes body weight loss. Interestingly, exercise training reduced the TGF-β1 expression and IkB-α ser32 phosphorylation in the hypothalamus of Middle-Aged obese mice. Taken together our study demonstrated that chronic exercise suppressed the TGF-β1/IkB-α axis in the hypothalamus and improved the energy homeostasis in an animal model of obesity-associated to aging.

SUBMITTER: Silva VRR

PROVIDER: S-EPMC5611986 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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Chronic exercise reduces hypothalamic transforming growth factor-β1 in middle-aged obese mice.

Silva Vagner R R VRR Katashima Carlos K CK Lenhare Luciene L Silva Carla G B CGB Morari Joseane J Camargo Rafael L RL Velloso Licio A LA Saad Mario A MA da Silva Adelino S R ASR Pauli Jose Rodrigo JR Ropelle Eduardo Rochete ER

Aging 20170801 8

Obesity and aging are associated with hypothalamic inflammation, hyperphagia and abnormalities in the thermogenesis control. It has been demonstrated that the association between aging and obesity induces hypothalamic inflammation and metabolic disorders, at least in part, through the atypical hypothalamic transforming growth factor-β (TGF-β1). Physical exercise has been used to modulate several metabolic parameters. Thus, the aim of this study was to evaluate the impact of chronic exercise on T ...[more]

PMID: 28854149

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Project description:BackgroundAlcohol (ALC) diminishes gonadotropin-releasing hormone (GnRH) secretion and delays puberty. Glial transforming growth factor β1 (TGFβ1) plays a role in glial-neuronal communications facilitating prepubertal GnRH secretion. We assessed the effects of acute ALC administration on TGFβ1-induced GnRH gene expression in the brain preoptic area (POA) and release of the peptide from the medial basal hypothalamus (MBH). Furthermore, we assessed actions and interactions of TGFβ1 and ALC on an adhesion/signaling gene family involved in glial-neuronal communications.MethodsPrepubertal female rats were administered ALC or water via gastric gavage at 7:30 am. At 9:00 am, saline or TGFβ1 (100 ng/3 μl) was administered into the third ventricle. At 3:00 pm, the POA was removed and frozen for gene expression analysis and repeated for protein assessments. In another experiment, the MBH was removed from ALC-free rats. After equilibration, tissues were incubated in Locke's medium only or medium containing TGFβ1 with or without 50 mM ALC for measurement of GnRH peptide released in vitro.ResultsTGFβ1 induced GnRH gene expression in the POA, and this effect was blocked by ALC. We also described the presence and responsiveness of the TGFβ1 receptor in the POA and showed that acute ALC exposure not only altered the TGFβ1-induced increase in TGFβ-R1 protein expression but also the activation of receptor-associated proteins, Smad2 and Smad3, key downstream components of the TGFβ1 signaling pathway. Assessment of an adhesion/signaling family consisting of glial receptor protein tyrosine phosphatase beta and neuronal contactin-associated protein-1 (Caspr1) and contactin showed that the neuronal components were induced by TGFβ1 and that ALC blocked these effects. Finally, TGFβ1 was shown to induce release of the GnRH peptide in vitro, an action that was blocked by ALC.ConclusionsWe have demonstrated glial-derived TGFβ1 induces GnRH gene expression in the POA and stimulates release of the peptide from the MBH, actions necessary for driving the pubertal process. Importantly, ALC acted at both brain regions to block stimulatory effects of TGFβ1. Furthermore, ALC altered neuronal components of an adhesion/signaling family previously shown to be expressed on GnRH neurons and implicated in glial-GnRH neuronal communications. These results further demonstrate detrimental effects of ALC at puberty.

Project description:BackgroundLeptin is one of the major adipokines in obesity that indicates the severity of fat accumulation. It is also an important etiological factor of consequent cardiometabolic and autoimmune disorders. Aging has been demonstrated to aggravate obesity and to induce leptin resistance and hyperleptinemia. Hyperleptinemia, on the other hand, may promote the development of age-related abnormalities. While major weight loss has been demonstrated to ameliorate hyperleptinemia, obese people show a poor tendency to achieve lasting success in this field. The question arises whether training intervention per se is able to reduce the level of this adipokine.ObjectivesWe aimed to review the literature on the effects of training intervention on peripheral leptin level in obesity during aging, in order to evaluate the independent efficacy of this method. In the studies that were included in our analysis, changes of adiponectin levels (when present) were also evaluated.Data sources3481 records were identified through searching of PubMed, Embase and Cochrane Library Database. Altogether 19 articles were suitable for analyses.Study eligibility criteriaEmpirical research papers were eligible provided that they reported data of middle-aged or older (above 45 years of age) overweight or obese (body mass index above 25) individuals and included physical training intervention or at least fitness status of groups together with corresponding blood leptin values.Statistical methodsWe used random effect models in each of the meta-analyses calculating with the DerSimonian and Laird weighting methods. I-squared indicator and Q test were performed to assess heterogeneity. To assess publication bias Egger's test was applied. In case of significant publication bias, the Duval and Tweedie's trim and fill algorithm was used.ResultsTraining intervention leads to a decrease in leptin level of middle-aged or older, overweight or obese male and female groups, even without major weight loss, indicated by unchanged serum adiponectin levels. Resistance training appears to be more efficient in reducing blood leptin level than aerobic training alone.ConclusionsPhysical training, especially resistance training successfully reduces hyperleptinemia even without diet or major weight loss.

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Chronic exercise reduces hypothalamic transforming growth factor-β1 in middle-aged obese mice.

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Chronic exercise reduces hypothalamic transforming growth factor-β1 in middle-aged obese mice.

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