Exercise and dietary change ameliorate high fat diet induced obesity and insulin resistance via mTOR signaling pathway

Bae, Ju Yong; Shin, Ki Ok; Woo, Ji Eun; Woo, Sang Heon; Jang, Ki Soeng; Lee, Yul Hyo; Kang, Sunghwun

doi:10.20463/jenb.2016.06.20.2.4

Cited by 17 publications

(22 citation statements)

References 39 publications

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“…Regular exercise and caloric restriction are effective treatments for the regulation of body weight [17, 18]. In this study, as expected, HFD increased fat mass and body weight, but regular exercise without a caloric restriction inhibited the increase in weight gain.…”

Section: Discussionsupporting

confidence: 79%

The effects of detraining and training on adipose tissue lipid droplet in obese mice after chronic high-fat diet

et al. 2017

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BackgroundIt is well known that exercise promotes lipolysis by stimulating the lipid droplet (LD) signaling pathway. However, few studies have been conducted to examine the effect of detraining with high fat diet (HFD) and training effects after long-term HFD. Here, we investigated the effect of detraining and training on adipose tissue LD pathway in diet-induced obese mice after continuous HFD.MethodsSeventy male C57BL/6 mice were randomly assigned into a Normal diet + Sedentary group (ND, n = 10) or a High-fat diet + Sedentary group (HF, n = 50); in the HF group, obesity was induced by a 45% fat chow for six weeks. For the subsequent eight weeks, the HF group was randomly subdivided into an HF (n = 30) or an HF + training group (HFT, n = 20), and the HFT group was subjected to treadmill training while on an HFD. Following this eight-week period, the HFT group stopped exercising (HFT-DT group, n = 10), and the mice in the HF group were randomly subdivided into an HF (n = 10) or an HF + training group (HF-T, n = 10). After training and detraining, abdominal visceral fat was obtained and analyzed by histological staining and western blot.ResultsTreadmill exercise decreased body weight and fat mass (P <0.05), and increased the levels of PKA, perilipin1, CGI-58, ATGL, and HSL (P <0.05) after eight weeks of training. Following eight weeks of detraining, the levels of PKA and HSL were decreased (P <0.05); however, exercise after chronic HFD increased the levels of PKA, perilipin1, CGI-58, ATGL, and HSL (P <0.05), and decreased body weight and fat mass (P <0.05).ConclusionsRegardless of dietary restrictions, exercise is an effective treatment for obesity, owing to the regulation of LD signaling proteins. Moreover, the effects of regular exercise after chronic HFD were similar to those of exercise in the absence of HFD. Therefore, although obesity is induced by chronic HFD, exercise without dietary change is sufficiently effective for obesity treatment regardless of the preceding HFD period.

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Section: Discussionsupporting

confidence: 79%

The effects of detraining and training on adipose tissue lipid droplet in obese mice after chronic high-fat diet

et al. 2017

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“…The mTOR/S6K1 pathway regulates the serine phosphorylation of IRS-1, and previous studies have showed that the increased phosphorylation of mTOR and S6K1 caused subcellular redistribution of IRS-1 and inactivation of IRS-1 by increasing its serine phosphorylation, leading to insulin resistance [27, 29, 30]. It has been reported by Bae et al [31] that exercise and dietary change stimulate the mTOR signaling pathway and ameliorate insulin resistance. Here, we found an increased phosphorylation of the mTOR/S6K1 pathway in the muscle cells after colorectal resection, while POC suppressed the activation of the mTOR/S6K1 pathway, and PIR was reduced.…”

Section: Discussionmentioning

confidence: 99%

Preoperative Oral Carbohydrate Reduces Postoperative Insulin Resistance by Activating AMP-Activated Protein Kinase after Colorectal Surgery

Shi

Yang

et al. 2020

Dig Surg

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Background: Postoperative insulin resistance (PIR) is a common response after colorectal surgery and an independent risk factor for recovery. Preoperative oral carbohydrate (POC) has been known to reduce PIR. Herein, we investigated whether its mechanism of action involves AMP-activated protein kinase (AMPK) and mTOR/S6K1/insulin receptor substrate-1 (IRS-1) pathways. Methods: Patients undergoing colorectal cancer resection were randomly assigned to a POC, fasting, or placebo group. The exclusion criteria were association with diseases or intake of medication affecting insulin sensitivity. Pre-and postoperative insulin resistance, and protein phosphorylation of AMPK, mTOR, and IRS-1 in the rectus abdominis muscle were evaluated. Results: From January 2017 to December 2017, 70 patients were randomized and 63 were evaluated. No difference was found in the clinical and operative characteristics among the 3 groups. In the POC group, the levels of blood glucose, blood insulin, and homeostasis model assessment of insulin resistance were significantly lower in the POC group than the fasting and placebo groups, and the insulin sensitivity index was significantly higher. The phosphorylation of AMPK in the POC group was significantly higher than that in the other 2 groups, whereas the phosphorylation of mTOR and IRS-1 was significantly lower. Conclusion: PIR involves AMPK and mTOR/S6K1/IRS-1 pathways. POC reduces PIR by the stimulation of AMPK, which suppresses the phosphorylation of mTOR/IRS-1 and attenuates PIR after colorectal resection.

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“…3). Strong evidence from preclinical studies has emerged to demonstrate that caloric restriction reduces obesity-related hyperactivation of mTOR complex 1 (mTORC1) in multiple tissues, including colon, pancreas and liver, in obese mice 55 , with diet and/or exercise interventions in mice and rats supporting these findings 137,138 . Exercise interventions in mice also demonstrated decreased kinase activity of mTOR in tumours of the liver 139 , suggesting that energy balance interventions have the potential to decrease tumour cell proliferation via the mTOR signalling pathway.…”

Section: Biological Mechanismsmentioning

confidence: 99%

Energy balance and gastrointestinal cancer: risk, interventions, outcomes and mechanisms

Ulrich

Himbert

Holowatyj

et al. 2018

Nat Rev Gastroenterol Hepatol

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Obesity increases the risk of multiple gastrointestinal cancers and worsens disease outcomes. Conversely, strong inverse associations have emerged between physical activity and colon cancer and possibly other gastrointestinal malignancies. The effect of weight loss interventions - such as modifications of diet and/or physical activity or bariatric surgery - remains unclear in patients who are obese and have gastrointestinal cancer, although large clinical trials are underway. Human intervention studies have already shed light on potential mechanisms underlying the energy balance-cancer relationship, with preclinical models supporting emerging pathway effects. Central to interventions that reduce obesity or increase physical activity are pluripotent cancer-preventive effects (including reduced systemic and adipose tissue inflammation and angiogenesis, altered adipokine levels and improved insulin resistance) that directly interface with the hallmarks of cancer. Other mechanisms, such as DNA repair, oxidative stress and telomere length, immune function, effects on cancer stem cells and the microbiome, could also contribute to energy balance effects on gastrointestinal cancers. Although some mechanisms are well understood (for instance, systemic effects on inflammation and insulin signalling), other areas remain unclear. The current state of knowledge supports the need to better integrate mechanistic approaches with preclinical and human studies to develop effective, personalized diet and exercise interventions to reduce the burden of obesity on gastrointestinal cancer.

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Exercise and dietary change ameliorate high fat diet induced obesity and insulin resistance via mTOR signaling pathway

Cited by 17 publications

References 39 publications

The effects of detraining and training on adipose tissue lipid droplet in obese mice after chronic high-fat diet

The effects of detraining and training on adipose tissue lipid droplet in obese mice after chronic high-fat diet

Preoperative Oral Carbohydrate Reduces Postoperative Insulin Resistance by Activating AMP-Activated Protein Kinase after Colorectal Surgery

Energy balance and gastrointestinal cancer: risk, interventions, outcomes and mechanisms

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