Modulation of Adipocytokines Response and Weight Loss Secondary to a Hypocaloric Diet in Obese Patients by -55CT Polymorphism of UCP3 Gene
Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, Valladolid, Spain-RD 056/0013.Hormone and Metabolic Research (Impact Factor: 2.12). 03/2008; 40(3):214-8. DOI: 10.1055/s-2008-1046796
Decreased expression or function of UCP3 (uncoupling protein 3) could reduce energy expenditure and increase the storage of energy as fat. Some studies have pointed to a role of UCP3 in the regulation of whole body energy homeostasis, diet induced obesity, and regulation of lipids as metabolic substrates. The C/C genotype of a polymorphism in the UCP3 promoter (-55C-->T) is associated with an increased expression of UCP3 mRNA in muscle. The aim of our study was to investigate the influence of -55CT polymorphism of UCP3 gene on adipocytokines response and weight loss secondary to a hypocaloric diet in obese patients. A population of 107 obese (body mass index >30) nondiabetic outpatients was analyzed in a prospective way. Before and after three months of a hypocaloric diet, an indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure, a serial assessment of nutritional intake with 3-day written food records, and biochemical analysis were performed. The lifestyle modification program consisted of a hypocaloric diet (1520 kcal, 52% of carbohydrates, 25% of lipids and 23% of proteins). The exercise program consisted of aerobic exercise for at least 3 times per week (60 minutes each). The mean age was 49.5+/-34.5 years and the mean BMI 34.5+/-4.8, with 27 males (25.3%) and 80 females (74.7%). Ninety patients (25 males/65 females) (83.6%) had the genotype 55CC (wild group) and 17 patients (2 male/15 females) (16.4%) 55CT (mutant group). The percentage of responders (weight loss) was similar in both groups (wild group: 84.7% vs. mutant group: 81.8%). BMI, weight, fat mass, systolic blood pressure, LDL cholesterol, waist circumference, and waist-to-hip ratio decreased in the wild group and RMR and VO (2) were increased. In the mutant group, BMI and weight decreased. Leptin and IL-6 levels have a significant decrease in the wild group (9.6%: p<0.05) and (30.5%: p<0.05), respectively. Patients with -55CC genotype have a significant decrease in leptin, interleukin 6, BMI, weight, fat mass, systolic blood pressure, LDL cholesterol, waist circumference, waist-to-hip ratio weight, fat mass, and systolic blood pressure.
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- "Interestingly, the ADRB3 Trp64Arg polymorphism may affect the regional distribution of fat loss (Nakamura et al., 2000), and could impair the capacity to lose visceral adipose tissue in response to prolonged caloric restriction (Tchernof et al., 2000). Different mutations in the uncoupling protein genes, such as UCP1 at -3826A/G position or rs1800592 (Nagai et al., 2011), UCP2 insertion/deletion (Mutombo, Yamasaki, & Shiwaku, 2013;Papazoglou et al., 2012) and UCP3 -55CT (rs1800849) carriers (De Luis, Aller, Izaola, Sagrado, & Conde, 2008b), may also result in differences in weight loss due to the genotype. On the other hand, other trials that investigated Trp64Arg variation (rs4994) in the ADRB3 gene (De Luis, Gonz alez Sagrado, Aller, Izaola, & Conde, 2009;Sakane et al., 1997;Yamakita, Ando, Tang, & Yamagata, 2010), as well as the Arg16Gly polymorphism (rs1042713) of ADRB2 gene (Sakane, Yoshida, Umekawa, Kogure, & Kondo, 1999) have shown a majority of results in favor of a role in weight resistance under energy deficit but with one exception (Lee, Kawakubo, Inoue, & Akabayashi, 2006). "
ABSTRACT: A personalized nutritional approach, based not only on phenotypic traits but also on genetic make-up, may help to control body weight and obesity. Recent advances in nutrigenetics, bioinformatics and genome-wide association/metabolomic/metagenomic studies are set to unleash a revolution in personalized nutrition. This article performs a systematic review of nutrigenetic data concerning single nucleotide polymorphisms (SNPs) involved in weight loss that are considered polygenic. SNPs located in or near FTO, MC4R, MC3R, POMC, LEP, LEPR, PLIN1, APOA5, LIPC, FABP2, INSIG2, IRS1, GIPR, ADBR2, ADRB3, UCP1, RETN, ADIPOQ, IL6, PPARG, TCF7L2, and CLOCK, among others, are comprehensively reviewed.
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ABSTRACT: Adiponectin is an adipose tissue-specific hormone that is commonly decreased in obese subjects. Furthermore, single-nucleotide polymorphisms (SNPs) of the adiponectin gene have been associated with metabolic phenotypes. The present study investigated whether the adiponectin gene promoter variant -11391 G/A (rs17300539) could predict the risk of developing traits characterizing the metabolic syndrome (MetS) and the impact of weight management. The -11391 G/A SNP was genotyped in 180 Spanish volunteers (BMI: 31.4+/-3.2 kg/m (2); age: 35+/-5 years). Clinical measurements were determined at baseline, following an 8-week low-calorie diet (LCD), and at 32 and 60 weeks. At baseline, the GG genotype was associated with higher HOMA-IR, insulin and triacylglyceride concentrations than other genotypes (p<0.05) and was also related with a higher risk of insulin resistance (OR: 2.437, p=0.025) and MetS clinical manifestations (OR: 3.236, p=0.003). Following the LCD, the increased risk in GG subjects compared with others disappeared (p>0.05). By 32 weeks after dietary therapy (n=84), GG carriers had recovered the risk of metabolic comorbidities (OR: 2.420, p=0.043). This risk was even more evident after 60 weeks (OR: 2.875, p=0.014). These data show an increased risk of insulin resistance and MetS complications in obese subjects of the -11391 GG genotype. The risk was markedly reduced during an energy-restricted diet, but was not sustained. Carriage of the A allele therefore confers protection from weight regain, and the effect is particularly evident 32-60 weeks after the dietary intervention, when improvement in GG subjects had disappeared.
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ABSTRACT: We examine how a public health genomics framework can be used to move genomic discoveries into clinical and public health practice for obesity prevention and treatment. There are four phases of translational research: T1: discovery to candidate health application; T2: health application to evidence-based practice guidelines; T3: practice guidelines to health practice; and T4: practice to population health impact. Types of multidisciplinary research and knowledge synthesis needed for each phase, as well as the importance of developing and disseminating evidence-based guidelines, are discussed. Because obesity genomics research is mostly in the discovery phase or in the very early phases of translation (T1), the authors present this framework to illustrate the range of translation activities needed to move genomic discoveries in obesity to actual applications that reduce the burden of obesity at the population level.
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