Associations of nicotidamide-N-methyltransferase, FTO, and IRX3 genetic variants with body mass index and resting energy expenditure in Mexican subjects.
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ABSTRACT:
SUBMITTER: Banales-Luna M
PROVIDER: S-EPMC7351746 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature
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Associations of nicotidamide-N-methyltransferase, FTO, and IRX3 genetic variants with body mass index and resting energy expenditure in Mexican subjects.
Bañales-Luna Maciel M Figueroa-Vega Nicté N Marín-Aragón Carolina Ivet CI Perez-Luque Elva E Ibarra-Reynoso Lorena L Gallardo-Blanco Hugo L HL López-Aguilar Itzel I Malacara Juan Manuel JM
Scientific reports 20200710 1
The enzyme nicotidamide-N-methyltransferase (NNMT) regulates adipose tissue energy expenditure through increasing nicotinamide adenosine dinucleotide (NAD<sup>+</sup>) content. NNMT methylates nicotinamide to N<sup>1</sup>-methylnicotidamide (MNA-1) using S-adenosyl methionine. The rs694539 NNMT polymorphism is associated with non-alcoholic steatohepatitis, and rs1941404 is associated with hyperlipidemia. The rs1421085 FTO is related to poor eating behaviors, and rs3751723 IRX3 is associated wit ...[more]
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Project description:Abstract In obesity the NNMTrs694539 polymorphism associates with cardiovascular damage and nonalcoholic steatohepatitis, and rs1941404 with hyperlipidemia.NNMT (Nicotidamide-N-methyltransferase) is a regulator of adiposity and energy expenditure correlating with BMIand energy metabolism. FTOrs1421085 polymorphism regulates food behavior, and IRX3rs3751723 is associated with obesity risk.Resting energy expenditure (REE) is an essential component of obesity. To evaluate the role of NNMTrs694539 and rs1941404,and FTOrs1421085 and IRX3rs3751723 polymorphisms on REEand BMI. We recruited 200 healthy subjects 30 to 50 years of age, 100 non-obese (BMI 18.5-29.5) and 100 obese (BMI ≥30 kg/m2). and REE evaluated by indirect calorimetry. A fasting blood sample was obtained for metabolites and DNA extraction. Leptin and insulin were quantified. MNA-1 was measured by LC-MS. The NNMTrs694539, rs1941404, FTOrs1421085, and IRX3rs3751723 polymorphisms were genotyped by PCR-RFLP and Taqman allelic discrimination respectively. MNA-1 concentrations and REE were higher in obese subjects. REE correlated with BMI, (p < 0.00001), insulin (p=0.001) andHOMA-IR (p=0.0004). The plasma MNA-1 correlated negatively with HOMA-IR in obese subjects (p=0.042). The rs694539AA genotype frequency was significantly higher in lean subjects. The NNMTrs1941404, and IRX3 rs3751723 polymorphisms was not different in allelic or genotypes frequencies in both groups. The risk allele frequency of FTOrs1421085 was different between groups (p=0.049; OR=1.76). Carriers of one or two risk alleles had more weight 6 kg or 2 BMI units than subjects with WT genotype. Under recessive model carriers of rs694539 AA genotype had lower weight, BMI, and REE than those with GG and AG genotypes, andcarriers of rs1941404GG genotype had marginally higher BMI, leptin, and MNA. The TG haplotype of rs1421085 and rs3751723 were associated with BMI adjusted by gender and age (coefficient -3.41±1.41, p=0.017). REE and MNA-1 were significant higher in obese subjects. Carriers of rs694539 AA genotype had lower weight, BMI, REE. The risk allele frequency of FTOrs1421085 was marginally different (p=0.049; OR=1.76) among groups. The carriers of one or two risk allele had 6 kg and 2 BMI units more than wild type genotype subjects. TG haplotype of rs1421085 and rs3751723 was associated with BMI. Support: CONACYT, and CIFOREA-UG.
| S-EPMC6550987 | biostudies-literature
Project description:Background: Asthma physiology affects respiratory function and inflammation, factors that may contribute to elevated resting energy expenditure (REE) and altered body composition. Objective: We hypothesized that asthma would present with elevated REE compared to weight-matched healthy controls. Methods: Adults with asthma (n = 41) and healthy controls (n = 20) underwent indirect calorimetry to measure REE, dual-energy X-ray absorptiometry (DEXA) to measure body composition, and 3-day diet records. Clinical assessments included spirometry, fractional exhaled nitric oxide (FENO), and a complete blood count. Results: Asthmatics had greater REE than controls amounting to an increase of ~100 kcals/day, even though body mass index (BMI) and body composition were similar between groups. Inclusion of asthma status and FENO in validated REE prediction equations led to improved estimates. Further, asthmatics had higher white blood cell (control vs. asthma (mean ± SD): 4.7 ± 1.1 vs. 5.9 ± 1.6, p < 0.01) and neutrophil (2.8 ± 0.9 vs. 3.6 ± 1.4, p = 0.02) counts that correlated with REE (both p < 0.01). Interestingly, despite higher REE, asthmatics reported consuming fewer calories (25.1 ± 7.5 vs. 20.3 ± 6.0 kcals/kg/day, p < 0.01) and carbohydrates than controls. Conclusion: REE is elevated in adults with mild asthma, suggesting there is an association between REE and the pathophysiology of asthma.
| S-EPMC8064324 | biostudies-literature
Project description:BackgroundEnergy restriction induces adaptations in resting energy expenditure (REE) and physical activity; inter-individual variability could be ascribed to genetic predisposition.The aim was to examine if changes in REE and physical activity as a result of weight loss were affected by candidate single nucleotide polymorphisms (SNPs).Methods148 subjects (39 men, 109 women), mean ± SD age: 41 ± 9 year; body mass index (BMI): 31.9 ± 3.0 kg/m2, followed a very low energy diet for 8 weeks. SNPs were selected from six candidate genes: ADRB2, FTO, MC4R, PPARG2, PPARD and PPARGC1A. REE (ventilated hood) and physical activity (tri-axial accelerometer) were assessed before and after the diet. General linear modelling included gender, age and additional relevant covariates for all parameters.ResultsThe heterozygotic genotype of FTO was associated with a higher amount of physical activity (1.71 Mcounts/d; CI 1.62-1.81) compared to the homozygotic major genotype (1.50 Mcounts/d; CI 1.40-1.59) (P < 0.001) while the homozygotic risk allele genotype was not different (1.56 Mcounts/d; CI 1.39-1.74) at baseline; moreover, a similar pattern was observed after energy restriction. Carrying the homozygotic minor genotype of ADRB2 was associated with a larger decrease in REE (P < 0.05) and greater adaptive thermogenesis (P < 0.05) after weight loss.ConclusionCarrying the minor ADRB2 allele homozygous was associated with a larger diet induced metabolic adaptation in energy expenditure and suggest a central role for reduced lipid mobilization. Carrying the risk allele of FTO homozygous was not associated with lower physical activity at baseline or after weight loss. Heterozygous carriers of one FTO risk allele showed greater physical activity before and after weight loss which might protect them in part from the higher obesity risk associated with FTO.
| S-EPMC7285957 | biostudies-literature
Project description:There is emerging evidence that circadian misalignment may alter energy expenditure, leading to obesity risk among those with irregular schedules [1-5]. It has been reported that energy expenditure is affected by the timing of sleep, exercise, and meals [6]. However, it is unclear whether the circadian system also modulates energy expenditure, independent of behavioral state and food intake. Here, we used a forced desynchrony protocol to examine whether fasted resting energy expenditure (REE) varies with circadian phase in seven participants. This protocol allowed us to uncouple sleep-wake and activity-related effects from the endogenous circadian rhythm, demonstrating that REE varies by circadian phase. REE is lowest at circadian phase ?0°, corresponding to the endogenous core body temperature (CBT) nadir in the late biological night, and highest at circadian phase ?180° in the biological afternoon and evening. Furthermore, we found that respiratory quotient (RQ), reflecting macronutrient utilization, also varies by circadian phase. RQ is lowest at circadian phase ?240° and highest at circadian phase ?60°, which corresponds to biological morning. This is the first characterization of a circadian profile in fasted resting energy expenditure and fasted respiratory quotient (with rhythmic profiles in both carbohydrate and lipid oxidation), decoupled from effects of activity, sleep-wake cycle, and diet in humans. The rhythm in energy expenditure and macronutrient metabolism may contribute to greater weight gain in shift workers and others with irregular schedules.
| S-EPMC6300153 | biostudies-literature
Project description:It is controversial whether weight loss reduces resting energy expenditure (REE) to a different magnitude in black and white women. This aim of this study was to determine whether changes in REE with weight loss were different between black and white postmenopausal women, and whether changes in body composition (including regional lean and fat mass) were associated with REE changes within each race. Black (n = 26) and white (n = 65) women (age = 58.2 +/- 5.4 years, 25 < BMI < 40 kg/m(2)) completed a 20-week weight-loss intervention. Body weight, lean and fat mass (total body, limb, and trunk) via dual-energy X-ray absorptiometry, and REE via indirect calorimetry were measured before and after the intervention. We found that baseline REE positively correlated with body weight, lean and fat mass (total, limb, and trunk) in white women only (P < 0.05 for all). The intervention decreased absolute REE in both races similarly (1,279 +/- 162 to 1,204 +/- 169 kcal/day in blacks; 1,315 +/- 200 to 1,209 +/- 185 kcal/day in whites). REE remained decreased after adjusting for changes in total or limb lean mass in black (1,302-1,182 kcal/day, P = 0.043; 1,298-1,144 kcal/day, P = 0.006, respectively), but not in white, women. Changes in REE correlated with changes in body weight (partial r = 0.277) and fat mass (partial r = 0.295, 0.275, and 0.254 for total, limb, and trunk, respectively; P < 0.05) independent of baseline REE in white women. Therefore, with weight loss, REE decreased in proportion to the amount of fat and lean mass lost in white, but not black, women.
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Project description:Pseudohypoparathyroidism type 1A (PHP1A) is caused by loss-of-function mutations on the maternally inherited GNAS allele and is associated with early-onset obesity, neurocognitive defects, and resistance to multiple hormones. The role of energy intake vs central regulation of energy expenditure in the pathophysiology of obesity remains unclear.The aim of this study was to evaluate resting energy expenditure (REE) in participants with PHP1A.We assessed REE, biochemical, endocrine, and auxological status of 12 participants with PHP1A who had normal or elevated body mass index; controls were a cohort of 156 obese participants.This study took place at Children's Hospital in Philadelphia and Sick Children's Hospital in Toronto.REE as a percent of predicted REE was the outcome measure.PHP1A participants had normal endocrine status while receiving appropriate hormone replacement therapy, but had significantly decreased REE as a percent of predicted REE (using the modified Schofield equation).Our results are consistent with REE being the principal cause of obesity in PHP1A rather than it being caused by excessive energy intake or endocrine dysfunction.
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Project description:PurposeThe purpose of this study was: 1) To compare Resting energy expenditure (REE) in adult males with Becker's Muscular Dystrophy (BeMD, n = 21, 39 ±12 years) and healthy controls (CTRL, n = 12, 37 ±12 years) 2) Determine whether other physiological parameters correlate with REE in BeMD, and 3) Compare current prediction methods of REE with measured REE.MethodsREE was calculated via indirect calorimetry using continuous, expired gas analysis following an overnight fast. Fat free mass (FFM) and fat mass were measured by bioelectrical impedance. B-mode ultrasound measured Tibialis Anterior (TA) and Gastrocnemius Medialis (GM) anatomical cross sectional area (ACSA). The Bone Specific Physical Activity Questionnaire measured physical activity.ResultsNo difference in REE was found between CTRL and BeMD groups (1913 ±203 & 1786 ±324 Kcal respectively). Other physiological comparisons showed increased fat mass (+54%), decreased TA ACSA (-42%), increased GM ACSA (+25%) as well as reduced respiratory function (FVC -28%; FEV1-27%) in BeMD adults compared to controls. REE estimated from prediction equations (Schofield's) in Muscular Dystrophy were different from measured REE (P<0.05, bias = -728kcal), while the Mifflin equation was no different from measured REE (r2 = 0.58, Bias = -8kcal). Within the present BeMD, REE predicted from FFM (REE = FFM x 34.57-270; r2 = 0.85) and body mass (REE = BM x 15.65 + 421.5; r2 = 0.66), were not different from measured REE (bias equals 0 and 0.2kcals, respectively).ConclusionsDespite no differences in REE between CTRL and BeMD adults, increased fat masses highlights the requirement for explicit nutritional guidelines, as well as maintenance of physical activity levels, where possible. Prediction equations are frequently used in clinical settings, however these have been shown to be less accurate in BeMD; therefore, the equations proposed here should be used where possible.
| S-EPMC5218559 | biostudies-literature
Project description:Body mass in humans and animals is strongly associated with the rate of heat production as defined by resting energy expenditure (REE). Beginning with the ancient Greeks up to the present time, philosophers and scientists have endeavored to understand the nature and sources of bodily heat. Today we recognize that body mass consists of organs and tissues, each of which produces a specified amount of heat at rest. An individual organ's REE can now be estimated in vivo as the product of its assumed mass-specific metabolic rate and its imaging-derived mass; whole-body REE reflects the sum of organ and tissue metabolic rates. The sizes of organs and total body mass in adults are governed by two main factors, a person's stature or height, and their level of adiposity. With greater body size, as represented by adult height independent of adiposity, organs remain stable or increase in mass according to distinct "scaling" patterns. Similarly, with greater relative adiposity organs adaptively accommodate to the increase in imposed mechanical and metabolic loading conditions. Through a detailed analysis of these stature and adiposity effects, we show how classical statistical REE prediction models can be mechanistically understood at the anatomic body composition level.
| S-EPMC6410366 | biostudies-literature
Project description:BACKGROUND:There are significant variations in gestational weight gain, with many women gaining in excess of the Institute of Medicine guidelines. Unfortunately, efforts to improve appropriate gestational weight gain have had only limited success. To date, interventions have focused primarily on decreasing energy intake and/or increasing physical activity. Maternal resting energy expenditure, which comprises ?60% of total energy expenditure compared with the ?20% that comes from physical activity, may be an important consideration in understanding variations in gestational weight gain. OBJECTIVE:Our objective was to quantify the changes in resting energy expenditure during pregnancy and their relationship to gestational weight gain and body composition changes among healthy women. We hypothesized that greater gestational weight gain, and fat mass accrual in particular, are inversely related to variations in resting energy expenditure. STUDY DESIGN:We conducted a secondary analysis of a prospective cohort studied before conception and late pregnancy (34-36 weeks). Body composition (estimated using hydrodensitometry) and resting energy expenditure (estimated using indirect calorimetry) were measured. The relationship between the changes in resting energy expenditure and gestational weight gain and the change in fat mass and fat-free mass were quantified. Resting energy expenditure was expressed as kilocalories per kilogram of fat-free mass per day (kilocalories per kilogram of fat-free mass-1/day-1) and kilocalories per day. Correlations are reported as r. RESULTS:Among 51 women, preconception body mass index was 23.0 (4.7) kg/m2; gestational weight gain was 12.8 (4.7) kg. Preconception and late pregnancy resting energy expenditure (kilocalories per day) correlated positively with the change in fat-free mass (r = 0.37, P = .008; r = 0.51, P = .001). Late-pregnancy resting energy expenditure (kilocalories per kilogram of fat-free mass-1/day-1) was inversely associated with the change in fat mass (r = -0.34, P = .02) and gestational weight gain (r = -0.29, P = .04). From before pregnancy through late gestation, the increase in resting energy expenditure (kilocalories per day) correlated positively with the change in fat-free mass (r = 0.44, P = .002) and negatively with the change in fat mass (r = -0.27, P = .06). CONCLUSION:The change in resting energy expenditure from before conception through late gestation correlated positively with changes in fat-free mass but negatively with fat mass accrual. Women with smaller increases in resting energy expenditure across pregnancy had greater gestational weight gain, specifically more adipose tissue. These data suggest that resting energy expenditure is an important factor in gestational weight gain, particularly excess fat mass accrual. Future lifestyle intervention studies need to consider clinically feasible means of estimating resting energy expenditure and, in response, tailor nutrient intake and composition recommendations. Implementing and testing such interventions would be a novel approach to improve compliance with gestational weight gain guidelines.
| S-EPMC5614817 | biostudies-literature
Project description:Children undergoing hematopoietic SCT (HSCT) typically receive parenteral nutrition (PN) due to gastrointestinal toxicities. Accurate determination of resting energy expenditure (REE) may facilitate optimal energy provision and help avoid unintended overfeeding or underfeeding. A multicenter, prospective cohort study of children undergoing allogeneic HSCT was performed, in which REE was measured by indirect calorimetry at baseline and twice weekly until 30 days after transplantation. Change in percent predicted REE over time from admission was analyzed using repeated measures regression analysis. In all, 26 children (14 females) with a mean (s.d.) age of 14.9 (4.2) years who underwent an HLA-matched sibling or unrelated donor transplantation were enrolled. Mean (s.d.) percent predicted REE at baseline was 92.4 (15.2). Baseline REE was highly correlated with lean body mass measured by dual energy X-ray absorptiometry (r=0.78, P<0.0001). REE decreased significantly over time, following a quadratic curve to a nadir of 79% predicted at 14 days post transplantation (P<0.001) and returned to near baseline by day 30. Children undergoing HSCT exhibit a significant reduction in REE in the early weeks after transplantation, a phenomenon that places them at risk for overfeeding. Serial measurements of REE or reductions in energy intake should be considered when PN is the primary mode of nutrition.
| S-EPMC3366174 | biostudies-literature