4 research outputs found
RESTING PLASMA AgRP LEVELS RESPONSE TO EXERCISE-CONJUGATED DIET AND ONLY DIET IN OVERWEIGHT AND OBESE SEDENTARY FEMALES
No full textAgouti-related peptide (AgRP) is an orexigenic neuropeptide produced mainly in the arcuate nucleus (ARC) of the hypothalamus, which leads to positive energy balance. The purpose of the present study was to investigate the resting plasma AgRP levels’ response to exercise-conjugated diet and only diet in overweight and obese sedentary female college students. Thirty subjects were randomly divided into two experimental groups and one control group. Experimental group 1 experienced 12 days of researchers’ proposed diet (D), experimental group 2 experienced 12 days of researchers’ proposed diet (every day) with 12-day running training (the intensity was 60 to 70�0heart rate maximum for 50 minutes) every other day (AED) and the control group remained sedentary with a normal diet in this period. Blood samples were collected 24 hours before and after the enforced protocol. Body fat percentage (BF�20of subjects was measured using the 3-point method. Plasma AgRP levels were measured using the enzyme-linked immunosorbent assay (ELISA) method. The data were analysed by Leven, Kolmogorov-Smirnov, one-way analysis of variance (ANOVA) and Tukey post-hoc test. At the end of the protocols, the resting plasma AgRP in the D group increased significantly (p0.05). Body weight and BMI were significantly reduced for both experimental groups (P<0.001). Body fat percentage in the AED group was decreased (p<0.001) and no change was observed in the D group. The present results indicate that the AED is better than the D protocol because it leads to stability of AgRP, which may prevent lipogenesis and ultimately reduce body fat percentage
High intensity interval exercise alters muscle IL-18, FNDC5, and hepatic MMPs in animal model of steatosis: Evidence of skeletal muscle—liver crosstalk
No full textSteatosis is a common disease worldwide. High intensity interval training (HIIT) may ameliorate steatosis, possibly through interactions between skeletal muscle and liver; however, mechanistic pathways are poorly understood. We aimed to determine potential mechanisms involved in skeletal muscle-liver crosstalk by measuring the gene expression of skeletal muscle interlukin-18 (IL-18) and fibronectin type III domain-containing protein 5 (FNDC5) and hepatic matrix metalloproteinase 2 (MMP-2) and 9 (MMP-9). Thirty-two adult male Wistar rats were randomly divided into four group including normal control (C), high intensity interval training (HIIT), hepatic steatosis+ HIIT (HS+HIIT) and sedentary hepatic steatosis (SHS). HIIT was performed 5 days per week for 5 weeks. Tetracycline (140 mg/kg) was administered by gavage for 7 days to induce NAFLD. We found that HIIT and HS+HIIT increased skeletal muscle expression of FNDC5 relative to SHS group but the increase was attenuated in HS+HIIT. SHS increased muscle IL-18 expression relative to HIIT, HS+HIIT, and C. Expression of hepatic MMP-2 and MMP-9 increased significantly in SHS in comparison with C. There was a significant increase in MMP-9 in HIIT compared with C. Moreover, hepatic MMP-9 expression decreased in both HIIT and SHS+HIIT relative to SHS. MMP-2 decreased significantly in HIIT compared with SHS. Furthermore, muscle IL-18 gene expression was significantly associated with gene expression of hepatic MMP-2 and MMP-9. We conclude that HIIT-induced alteration of skeletal muscle-derived myokines may alter the gene expression of hepatic matrix metalloproteinases, collagenases involved in pathogenesis of liver diseases. Furthermore, steatosis may possibly influence myokine profiles in skeletal muscle. Accordingly, skeletal muscle-liver crosstalk is possibly targeted by HIIT and steatosis in terms of therapeutic approach
Signals from the Adipose Microenvironment and the Obesity–Cancer Link—A Systematic Review
No full textAbstract
Obesity and its associated metabolic dysregulation are established risk factors for many cancers. However, the biologic mechanisms underlying this relationship remain incompletely understood. Given the rising rates of both obesity and cancer worldwide, and the challenges for many people to lose excess adipose tissue, a systematic approach to identify potential molecular and metabolic targets is needed to develop effective mechanism-based strategies for the prevention and control of obesity-driven cancer. Epidemiologic, clinical, and preclinical data suggest that within the growth-promoting, proinflammatory microenvironment accompanying obesity, crosstalk between adipose tissue (comprised of adipocytes, macrophages and other cells) and cancer-prone cells may occur via obesity-associated hormones, cytokines, and other mediators that have been linked to increased cancer risk and/or progression. We report here a systematic review on the direct “crosstalk” between adipose tissue and carcinomas in humans. We identified 4,641 articles with n = 20 human clinical studies, which are summarized as: (i) breast (n = 7); (ii) colorectal (n = 4); (iii) esophageal (n = 2); (iv) esophageal/colorectal (n = 1); (v) endometrial (n = 1); (vi) prostate (n = 4); and (vii) ear-nose-throat (ENT) cancer (n = 1). Findings from these clinical studies reinforce preclinical data and suggest organ-dependent crosstalk between adipose tissue and carcinomas via VEGF, IL6, TNFα, and other mechanisms. Moreover, visceral white adipose tissue plays a more central role, as it is more bioenergetically active and is associated with a more procancer secretome than subcutaneous adipose tissue. Efforts to eavesdrop and ultimately interfere with this cancer-enhancing crosstalk may lead to new targets and strategies for decreasing the burden of obesity-related cancers. Cancer Prev Res; 10(9); 494–506. ©2017 AACR.</jats:p
