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Starch Digestion–Related Amylase Genetic Variant Affects 2-Year Changes in Adiposity in Response to Weight-Loss Diets: the POUNDS Lost Trial

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Starch Digestion–Related Amylase Genetic Variant Affects 2-Year Changes in Adiposity in Response to Weight-Loss Diets: the POUNDS Lost Trial 2416 Diabetes Volume 66, September 2017 Starch Digestion–Related Amylase Genetic Variant Affects 2-Year Changes in Adiposity in Response to Weight-Loss Diets: The POUNDS Lost Trial Yoriko Heianza,1 Dianjianyi Sun,1 Tiange Wang,1 Tao Huang,2 George A. Bray,3 Frank M. Sacks,4 and Lu Qi1,4,5 Diabetes 2017;66:2416–2423 | https://doi.org/10.2337/db16-1482 Salivary and pancreatic amylases (encoded by AMY1 and role in determining energy balance, which regulates body AMY2 genes, respectively) are responsible for digesting weight (BW) and adiposity (2,3). The digestion of polysac- starchy foods. AMY1 and AMY2 show copy number vari- charide carbohydrates begins in the mouth by action of ations that affect differences in amylase amount and activ- salivary a-amylase, which catalyzes the hydrolysis of the ity, and AMY1 copies have been associated with adiposity. a-1,4-glycosidic bonds of starch, followed by the action of We investigated whether genetic variants determining pancreatic amylase. Salivary a-amylase is encoded by the amylase gene copies are associated with 2-year changes salivary amylase gene (AMY1), which shows extensive copy in adiposity among 692 overweight and obese individuals number variations (4–7) that directly affect individual var- who were randomly assigned to diets varying in macro- iability in salivary amylase amount and activity (8–10) as nutrient content. We found that changes in body weight well as serum concentrations of total and pancreatic amy- (BW) and waist circumference (WC) were significantly dif- lase (11). AMY1 is located in a gene cluster (1p21.1) that ferent according to the AMY1-AMY2 rs11185098 genotype. also includes pancreatic amylase genes (AMY2A and Individuals carrying the A allele (indicating higher amylase AMY2B), and AMY1 and AMY2A copy numbers are signifi- OBESITY STUDIES amount and activity) showed a greater reduction in BW and WC at 6, 12, 18, and 24 months than those without the cantly correlated (6). AMY1 Aallele(P < 0.05 for all). The association was stronger for Increasing evidence suggests that low gene copy – long-term changes compared with short-term changes of numbers are associated with obesity (5,12 14), although fi these outcomes. The genetic effects on these outcomes did the ndings are not entirely consistent (7,15). In epidemi- not significantly differ across diet groups. In conclusion, the ological studies, low serum concentrations of amylase have genetic variant determining starch metabolism influences been associated with elevated BMI (16–19), waist circum- the response to weight-loss dietary intervention. Over- ference (WC) (16,20), or visceral adipose tissue area (21). weight and obese individuals carrying the AMY1-AMY2 Furthermore, studies have suggested that AMY1 copy num- rs11185098 genotype associated with higher amylase ac- beralsoplaysaroleinglucoseuptakeandglucosemetab- tivity may have greater loss of adiposity during low-calorie olism (11,22). A novel study compared AMY1 copy number diet interventions. of individuals of European ancestry from the 1000 Genomes Project with their single nucleotide polymorphism (SNP) genotypes and identified genetic variants associated with Dietary carbohydrates account for the greatest source of AMY1 copies (7). Such copy number variation of AMY1 energy intake in most human diets (1) and play an important likely is due to adaptation to diets rich in starchy food (4). 1Department of Epidemiology, School of Public Health and Tropical Medicine, Corresponding author: Lu Qi, [email protected]. Tulane University, New Orleans, LA Received 1 December 2016 and accepted 17 June 2017. 2Epidemiology Domain, Saw Swee Hock School of Public Health and Department Clinical trial reg. no. NCT00072995, clinicaltrials.gov. of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore © 2017 by the American Diabetes Association. Readers may use this article as 3Pennington Biomedical Research Center, Louisiana State University, Baton long as the work is properly cited, the use is educational and not for profit, and the Rouge, LA work is not altered. More information is available at http://www.diabetesjournals 4Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA .org/content/license. 5Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA diabetes.diabetesjournals.org Heianza and Associates 2417 We hypothesized that starch digestion–related amylase ge- 24 months or data on fasting glucose at 6 or 24 months netic variants affect the regulation of body adiposity, par- were included in the current analysis. The genotype fre- ticularly when the intake of polysaccharide, the substrate quency was not significantly different between individuals for amylase, is changed. We examined associations of with and without follow-up data. copy number related to AMY1-AMY2 genotype and 2-year Measurements and Selection of Amylase Gene SNP changes of adiposity in participants of the Preventing Over- weight Using Novel Dietary Strategies (POUNDS Lost) Height was measured at the baseline examination, and BW trial. POUNDS Lost is thus far one of the largest random- and WC were measured in the morning before break- ized dietary intervention trials on long-term weight loss fast at baseline and at 6, 12, 18, and 24 months during among overweight and obese individuals (23). We investi- the intervention. BW was measured by calibrated hospital gated whether the AMY1-AMY2 genotype rs11185098, scales, and WC was measured by using a nonstretchable which determines starch metabolism, influences long-term tape measure 4 cm above the iliac crest (24). BMI was weight-loss response to dietary intervention among over- calculated as weight in kilograms divided by the square of weight and obese individuals. We also investigated associa- height in meters. Fasting blood samples were obtained at tions of the AMY1-AMY2 genotype with changes in glucose baseline and 6 and 24 months, and fasting serum glucose metabolism in relation to weight loss. and insulin levels (Diagnostic Products Corporation) were measured at the clinical laboratory at the Pennington RESEARCH DESIGN AND METHODS Biomedical Research Center. HOMA for insulin resistance Study Participants (HOMA-IR) was calculated as described previously (25). The sample comprised 811 overweight and obese individ- Blood pressure was measured with the use of an automated ; uals randomly assigned to one of four energy-reduced diets device (HEM-907XL; Omron). A random sample of 50% of varying in macronutrient composition of fat, protein, and the total study participants were selected to undergo DEXA carbohydrates to compare the diets’ effects on BW change scans for the assessment of body composition (26). The over 2 years in the POUNDS Lost trial (23). The study was DEXA scan was performed with a Hologic QDR 4500A after conducted from October 2004 through December 2007 an overnight fast; total fat mass, total lean mass, whole-body at two sites: the Harvard T.H. Chan School of Public total percent fat mass, and trunk fat percent were measured Health and Brigham and Women’s Hospital in Boston, at baseline and 6 and 24 months during the intervention. Massachusetts, and the Pennington Biomedical Research DNA was extracted from the buffy coat fraction of Center of Louisiana State University System, in Baton centrifuged blood by using the QIAamp DNA Blood Mini Rouge, Louisiana. All participants gave written informed Kit (QIAGEN, Chatsworth, CA). A total of 799 participants consent. The study was approved by the human subjects were genotyped for 715,481 SNPs by using an Illumina fi committee at each institution and by a data and safety In nium OmniExpress-24 Kit. The genotype success rate monitoring board appointed by the National Heart, Lung, was 99%. After quality control (sample call rate $95%, SNP and Blood Institute. call rate $95%, P . 1.0E-6 for Hardy-Weinberg equilibrium The targeted percentages of energy derived from fat, test, minor allele frequency $0.01), the genotyped data protein, and carbohydrates in the four diets were 1) 20%, set had 727 samples and 660,673 SNPs. Because of the 15%, and 65%; 2) 20%, 25%, and 55%; 3) 40%, 15%, and potential population stratification and limited sample size 45%; and 4) 40%, 25%, and 35%, respectively. Two diets of non-European Hispanics (n = 24) and Asians (n = 11), were low fat (20%) and the other two high fat (40%), and 692 participants (583 whites and 109 blacks) had available two diets were average protein (15%) and the other two data for the current study. We used the Michigan Im- high protein (25%), which constituted a 2 3 2factorial putation Server (https://imputationserver.sph.umich.edu/ design. Major exclusion criteria were the presence of diabe- index.html) to impute SNPs on chromosomes 1–22, with tes or unstable cardiovascular disease, the use of medications 1000G Phase 3 v5 as the reference panel. In the current that affect BW, and insufficient motivation (23). More details study, we used an imputed SNP, rs11185098, with high of the study have been described in detail elsewhere (23). imputation quality (R2 $ 0.9). Selection of this SNP was The current study included 692 individuals with data on based on the variant that showed the strongest association the AMY1 variant SNP rs11185098 located in amylase (among all the SNPs presented) with obesity in the previous genes (AMY1, AMY2A,andAMY2B) at the baseline exami- study (7) and was the only SNP located near all three am- nation. Most of the individuals were considered normogly- ylase genes (AMY1, AMY2A,andAMY2B). In addition, the cemic on the basis of fasting glucose levels (93.8% had fasting minor allele frequency of this SNP was common, which glucose ,6.1 mmol/L, and 82.8% had ,5.5 mmol/L), and provided better power in the analysis (7). The minor (A) none of the study participants were regularly taking insulin allele of SNP rs11185098 was reported to be positively or oral hypoglycemic agents at the baseline examination.
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