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Browning formation markers of subcutaneous adipose tissue in relation to resting energy expenditure, physical activity and diet in humans© 2017 Walter de Gruyter GmbH, Berlin/Boston. Regular exercise and diet may contribute to white adipose tissue (WAT) conversion into a brown adipose-like phenotype that may increase resting energy expenditure (REE), leading to weight loss. We examined the relationship between REE, physical activity (PA) participation and diet with browning formation markers of subcutaneous WAT in healthy men. We assessed REE, diet and body composition of 32 healthy men [age (years): 36.06 ± 7.36, body mass index (BMI): 27.06 ± 4.62 (kg/m 2 )]. Participants also underwent measurements of PA [metabolic equivalent (MET)-min/week] using the International Physical Activity Questionnaire (IPAQ), while they undertook a subcutaneous fat biopsy from the abdominal region to assess the mRNA expressions of uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma (PPARγ). We found no associations between the UCP1, PGC-1α, PPARα and PPARγ mRNAs with REE, PA levels and diet (p > 0.05). However, the PGC-1α, PPARα and PPARγ mRNAs were more expressed in individuals displaying moderate rather than low PA levels (p < 0.05). Furthermore, PGC-1α, PPARα and PPARγ mRNAs were negatively correlated with fat mass percentage (p < 0.05). PGC-1α and PPARα mRNAs were also negatively correlated with BMI, while PGC-1α mRNA was inversely associated with waist-to-hip ratio (p < 0.05). REE, PA levels and diet are not associated with browning formation indices of subcutaneous adipose tissue in healthy adult men.
Thermogenic capacity of human white-fat: the actual pictureCold exposure and exercise may increase thermogenic capacity of white adipose tissue (WAT), which could subsequently enhance energy expenditure and body weight loss. We aimed to identify possible alterations in uncoupling protein 1 (UCP1)—the main biomarker of thermogenic activation—in human WAT due to both cold exposure and exercise, as well as the link between environmental temperature and thermogenic capacity of human WAT. MATERIAL & METHOD: We conducted four human experimental studies and two systematic reviews and meta-analyses—PROSPERO registration CRD42019120116, CRD42019120213. RESULTS: UCP1 mRNA was higher in winter than in summer [t(30) = 2.232, p = 0.03] in human WAT and our meta-analysis showed a main effect of cold exposure on human UCP1 mRNA [standard mean difference (Std-md) = 1.81, confidence interval (CI) = 0.50–3.13, p = 0.007]. However, UCP1 mRNA/protein expressions displayed no associations with %fat mass or BMI (p > 0.05, Cohen’s f2 < 0.20). Both a 2-hour cooling and a non-cooling protocol preceding the positron emission tomography/computed tomography (PET/CT) measurements revealed no association between environmental temperature and standardised uptake value (SUVmax) of human WAT, as well as no mean differences in SUVmax-WAT-activity between winter and summer. An 8-week exercise program had no effect on UCP1 of human WAT or on body composition. Our meta-analysis also revealed: (a) no effect of chronic exercise on human UCP1 mRNA, (b) a main effect of chronic exercise on UCP1 protein concentrations (Std-md = 0.59, CI = 0.03–1.16, p = 0.04) and UCP1 mRNA (Std-md = 1.76, CI = 0.48–3.04, p = 0.007) in WAT of normal diet animals, c) a main effect of chronic exercise on UCP1 mRNA (Std-md = 2.94, CI = 0.24–5.65, p = 0.03) and UCP1 protein concentrations (Std-md = 2.06, CI = 0.07–4.05, p = 0.04) of high-fat diet animals. CONCLUSIONS: Cold exposure represents a main stimulus for increased thermogenic capacity in human white adipocytes; however, this may have no impact on body weight loss. Chronic exercise may represent no major stimulus for UCP1 induced in human white adipocytes, while in animals it increases UCP1 gene independently of their diet. Therefore, evidence from animal studies regarding UCP1 gene activation in white adipocytes may not be applicable in humans. Finally, the identification of human WAT thermogenic capacity via PET/CT examination may be optimal with both a cooling and a non-cooling protocol.