Leptin and leptin receptor genetic variants associate with habitual physical activity and the arm body composition response to resistance training

Abstract

PURPOSE We investigated the influence of Leptin (LEP) and leptin receptor (LEPR) SNPs on habitual physical activity (PA) and body composition response to a unilateral, upper body resistance training (RT) program. METHODS European-derived American volunteers (men=111, women=131, 23.4±5.4 yr, 24.4±4.6 kg·m−2) were genotyped for LEP 19 G>A (rs2167270), and LEPR 326 A>G (rs1137100), 668 A>G (rs1137101), 3057 G>A (rs1805096), and 1968 G>C (rs8179183). They completed the Paffenbarger PA Questionnaire. Arm muscle and subcutaneous fat volumes were measured before and after 12wk of supervised RT with MRI. Multivariate and repeated measures ANCOVA tested differences among phenotypes by genotype and gender with age and body mass index as covariates. RESULTS Adults with the LEP 19 GG genotype reported more kcal/wk in vigorous intensity PA (1273.3±176.8, p=0.017) and sports/recreation (1922.8±226.0, p<0.04) than A allele carriers (718.0±147.2, 1328.6±188.2, respectively). Those with the LEP 19 GG genotype spent more hr/wk in light intensity PA (39.7±1.6) than A allele carriers (35.0±1.4, p=0.03). In response to RT, adults with the LEPR 668 G allele gained greater arm muscle volume (67687.05±3186.7 vs. 52321.87±5125.05 mm3, p=0.01) and subcutaneous fat volume (10599.89±3683.57 vs. −5224.73±5923.98 mm3, p=0.02) than adults with the LEPR 668 AA genotype, respectively. CONCLUSION LEP19 G>A and LEPR 668 A>G associated with habitual PA and the body composition response to RT. These LEP and LEPR SNPs are located in coding exons likely influencing LEP and LEPR function. Further investigation is needed to confirm our findings and establish mechanisms for LEP and LEPR genotype and PA and body composition associations we observed.

Heterogeneity in resistance training-induced muscle strength and mass responses in men and women of different ages

“…In previous studies with healthy human subjects, e.g., several genetic variations (Riechman et al 2004;Devaney et al 2009;Walsh et al 2012;Van Deveire et al 2012), differences in skeletal muscle gene Raue et al 2012;Phillips et al 2013) and microRNA expression (Davidsen et al 2011), phosphorylation status of signaling proteins (Mayhew et al 2011;Mitchell et al 2013), androgen receptor concentrations (Ahtiainen et al 2011;Mitchell et al 2013), and satellite cell count (Petrella et al 2008) have been suggested to segregate high and low responders to RTinduced muscle hypertrophy. The physiological aspects of individual variation in phenotype responses to RT are apparently very complex phenomena and more studies specifically focused on high and low responders are required to reveal unambiguously the mechanisms of individual differences in RT-induced adaptations.…”

Neonatal leptin deficiency reduces frontal cortex volumes and programs adult hyperactivity in mice

“…In our prior studies, neonatal leptin administration had robust effects on adult brain volumes, while complementary investigations have shown effects of adult leptin administration on frontal lobe development [13, 17]. Further linking leptin deficiency and locomotor activity are studies by Walsh and colleagues showing an association between leptin or leptin receptor genetic variants and physical activity [32]. The pegylated leptin antagonist utilized in the current investigations allowed potent, sustained central leptin deficiency that, just as importantly, is reversible within days of LX discontinuation [19], implicating postnatal days 4–14 as a critical window of leptin-modulated developmental susceptibility.…”

Contribution of body composition components and soft‐tissue biochemical factors to genetic variation of body mass index (BMI) in an ethnically homogeneous population

“…In addition, the genetic correlations between leptin and body composition, especially obesity are well known. Several genetic polymorphisms, mapped to a number of genes (e.g., LEP G (‐2548) A, A19G, LEPR G 668A, SERPINF1, and LRP1) have been proposed as possible factors involved in affecting leptin levels and in obesity regulation (Bohm et al, ; Franek et al, ; Smith et al, ; Walsh et al, ). However, the situation with other biochemical factors and body composition is probably even more complex.…”