有肥胖基因 想減磅都難過人？ 最後更新: 0502 15:54 / 建立時間: 0502 07:40 做極運動都無減磅，或是肥胖基因作怪。美國一項研究發現擁有較多肥胖基因人士做gym，減低體重的效果不顯之餘，反有增磅趨勢。本港專家認為這類人士減肥最好從飲食調控著手，再加上運動，才可以踢走脂肪。美國亞利桑那大學一項研究安排84名30至65歲女性參與健身訓練，包括不同體重的女性，每星期做3次gym，每次75分鐘，持續一年。研究同時分析受訪女性的肥胖基因數量，結果找到21個與肥胖有關的基因。分析發現，帶有較少肥胖基因的女性，完成健身訓練後，平均可減去3磅。相反，有較多肥胖基因者，反而增加2.6磅。研究人員估計，肥胖基因會令人容易肚餓，尤其運動後，故做gym後暴飲暴食的機率較高，認為有肥胖基因者要加倍努力才能減肥。香港中文大學內科及藥物治療學系名譽臨床副教授唐俊業指出，「減極都咁肥嘅人」過往多被指與新陳代謝慢有關，隨著基因研究發達，肥胖基因越揭越多，相信是元凶之一。人體每個基因的組合都不同，有些組合較容易令人肥胖，故被稱為「肥胖基因」。醫學界已知有些肥胖基因，可減慢熱量消耗速度，令人有「飲水都肥」的錯覺，也有肥胖基因讓人容易肚餓，以致食極唔飽。擁有肥胖基因人士因減磅難，故正確的飲食調控，比單靠運動消耗脂肪更重要，「食一碟炒麵或炒飯，已攝取過千卡路里，但一般人跑步半個鐘，先消耗到250卡路里，如果唔戒口，做幾多運動，先消耗到食多咗嘅熱量？」唐強調減肥人士要做到「能量負資產」才有減重效果，即每日從飲食吸收的能量，要比身體所需為少，才會燃燒儲存的脂肪。運動可增加肌肉力量，同樣不可缺少。要了解自己是否有肥胖基因，本港暫未有準確測試，或要到外國接受測試，惟費用不菲，加上肥胖基因研究的數據多用於外國人，測試未必適合亞洲人。
Genetic Factors May Affect Exercise Benefit UA Mel and Enid Zuckerman College of Public Health | May 1, 2015 Resistance training isn't necessarily futile for women with higher genetic risk of obesity, UA researchers point out. Those with lower risk simply might have more to gain. Resistance exercise has well-known health benefits, but the magnitude of those benefits may differ according to an individual's genetic make-up. Women with a high genetic risk of obesity may benefit less from resistance exercises than those at a lower genetic risk, according to research published in the International Journal of Obesity. "With the recent identification of body mass index–associated genetic variants, it is possible to investigate the interaction of these genetic factors with exercise on body composition outcomes," said lead researcher Yann Klimentidis, assistant professor of epidemiology at the University of Arizona's Mel and Enid Zuckerman College of Public Health. Klimentidis and colleagues analyzed genetic markers of 148 women between the ages of 30 and 65 years old who participated in a yearlong randomized trial called the Bone Estrogen and Strength Training, or BEST, study. During the trial, 84 participants were asked to engage in supervised, high-intensity resistance training and moderate-impact, weight-bearing exercises for 75 minutes, three days a week, for 12 months. During the trial, participants were asked to take calcium supplements, but not to change their diet otherwise, and dietary intake was recorded at random intervals. A genetic risk score for obesity for each participant then was calculated based on 21 genetic markers thought to affect body weight. The authors found that participants with a low genetic risk score for obesity benefited most from the exercise regimen, at least when it came to weight and body composition outcomes. This included a reduction in weight, total and percentage body fat, and abdominal fat. "This doesn't mean that resistance training is futile for women with higher genetic risk for obesity. It means those with lower genetic risk just benefited more," explains Jennifer Bea, assistant professor at the UA College of Medicine – Tucson. "We have previously shown that the resistance training was important for these women in many other ways, including improved bone density. Like most interventions, exercise is not a one-size-fits-all proposition. People with higher genetic risk scores for higher BMI may benefit more from aerobic training, for example." The study found weight-loss response to resistance exercise, including changes in body composition, differs according to an individual's genetic risk for obesity. The authors suggest that further studies in other populations be undertaken, with a focus on other health-related outcomes using other genetic variants. Further research also is needed to identify the molecular and physiological mechanisms that these genes are involved in, and to determine optimal weight-management strategies based on an individual's genetic profile. The BEST study was conducted by Timothy Lohman, professor emeritus in the Department of Physiology, and Scott Going, professor in the Department of Nutritional Sciences, at the UA.
Genetic studies of body mass index yield new insights for obesity biology Nature 518, 197–206 (12 February 2015) Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10−8), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ~2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.
High genetic-risk individuals benefit less from resistance exercise intervention International Journal of Obesity (30 April 2015)
Background/Objectives Genetic factors play an important role in body mass index (BMI) variation, and also likely play a role in the weight-loss and body composition response to physical activity/exercise. With the recent identification of BMI–associated genetic variants, it is possible to investigate the interaction of these genetic factors with exercise on body composition outcomes.
Subjects/Methods In a block-randomized clinical trial of resistance exercise among women (n=148), we examined whether the putative effect of exercise on weight and DXA-derived body composition measurements differs according to genetic risk for obesity. Approximately one-half of the sample was randomized to an intervention consisting of a supervised, intensive, resistance exercise program, lasting one year. Genetic risk for obesity was defined as a genetic risk score (GRS) comprised of 21 SNPs known to be associated with normal BMI variation. We examined the interaction of exercise intervention and the GRS on anthropometric and body composition measurements after one year of the exercise intervention.
Results We found statistically significant interactions for body weight (P=0.01), body fat (P=0.01), body fat % (P=0.02), and abdominal fat (P=0.02), whereby the putative effect of exercise is greater among those with a lower level of genetic risk for obesity. No single SNP appears to be a major driver of these interactions.
Conclusions The weight-loss response to resistance exercise, including changes in body composition, differs according to an individual's genetic risk for obesity.
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