Acute effects of active breaks during prolonged sitting on subcutaneous adipose tissue gene expression: an ancillary analysis of a randomised controlled trial.

Active breaks in prolonged sitting has beneficial impacts on cardiometabolic risk biomarkers. The molecular mechanisms include regulation of skeletal muscle gene and protein expression controlling metabolic, inflammatory and cell development pathways. An active communication network exists between adipose and muscle tissue, but the effect of active breaks in prolonged sitting on adipose tissue have not been investigated. This study characterized the acute transcriptional events induced in adipose tissue by regular active breaks during prolonged sitting. We studied 8 overweight/obese adults participating in an acute randomized three-intervention crossover trial. Interventions were performed in the postprandial state and included: (i) prolonged uninterrupted sitting; or prolonged sitting interrupted with 2-minute bouts of (ii) light- or (iii) moderate-intensity treadmill walking every 20 minutes. Subcutaneous adipose tissue biopsies were obtained after each condition. Microarrays identified 36 differentially expressed genes between the three conditions (fold change ≥0.5 in either direction; p < 0.05). Pathway analysis indicated that breaking up of prolonged sitting led to differential regulation of adipose tissue metabolic networks and inflammatory pathways, increased insulin signaling, modulation of adipocyte cell cycle, and facilitated cross-talk between adipose tissue and other organs. This study provides preliminary insight into the adipose tissue regulatory systems that may contribute to the physiological effects of interrupting prolonged sitting

Effects of breaking up prolonged sitting on skeletal muscle gene expression

Breaking up prolonged sitting has been beneficially associated with cardiometabolic risk markers in both observational and intervention studies. We aimed to define the acute transcriptional events induced in skeletal muscle by breaks in sedentary time. Overweight/obese adults participated in a randomized three-period, three-treatment crossover trial in an acute setting. The three 5-h interventions were performed in the postprandial state after a standardized test drink and included seated position with no activity and seated with 2-min bouts of light- or moderate-intensity treadmill walking every 20 min. Vastus lateralis biopsies were obtained in eight participants after each treatment, and gene expression was examined using microarrays validated with real-time quantitative PCR. There were 75 differentially expressed genes between the three conditions. Pathway analysis indicated the main biological functions affected were related to small-molecule biochemistry, cellular development, growth and proliferation, and carbohydrate metabolism. Interestingly, differentially expressed genes were also linked to cardiovascular disease. For example, relative to prolonged sitting, activity bouts increased expression of nicotamide N-methyltransferase, which modulates anti-inflammatory and anti-oxidative pathways and triglyceride metabolism. Activity bouts also altered expression of 10 genes involved in carbohydrate metabolism, including increased expression of dynein light chain, which may regulate translocation of the GLUT-4 glucose transporter. In addition, breaking up sedentary time reversed the effects of chronic inactivity on expression of some specific genes. This study provides insight into the muscle regulatory systems and molecular processes underlying the physiological benefits induced by interrupting prolonged sitting

Adipogenic differentiation of cultured human primary subcutaneous white adipocye precursor cells.

<p>(a) After differentiation cells were fixed and stained with oil red-O; images shown are 10x magnification. (b) Lipid content was measured by quantification of oil red-O staining (absorbance at 495 nm) (n = 4). After differentiation cells were treated with vehicle (Veh, PBS) or 0.5 mM N⁶,2′-O-Dibutyryladenosine 3′,5′-cyclic monophosphate (db-cAMP) for 6 hours, and glycerol secretion into media was measured to determine rates of lipolysis. Glycerol secretion increased significantly with db-cAMP compared to vehicle treatment, but there was no difference between groups (*P<0.05 db-cAMP <i>vs</i> veh, n = 5).</p

Fold-change in UCP1 protein content post-differentiation compared with pre-differentiation (n = 4, L; Lean, O; Obese; *P<0.05 vs pre-differentiation, † P<0.05 vs Obese post-differentiation, pre-differentiation normalized to 1.0).

<p>Fold-change in UCP1 protein content post-differentiation compared with pre-differentiation (n = 4, L; Lean, O; Obese; *P<0.05 vs pre-differentiation, † P<0.05 vs Obese post-differentiation, pre-differentiation normalized to 1.0).</p

Advanced glycation end products (AGEs) are cross-sectionally associated with insulin secretion in healthy subjects

It has been postulated that chronic exposure to high levels of advanced glycation end products (AGEs), in particular from dietary sources, can impair insulin secretion. In the present study, we investigated the cross-sectional relationship between AGEs and acute insulin secretion during an intravenous glucose tolerance test (IVGTT) and following a 75\ua0g oral glucose tolerance test (OGTT) in healthy humans. We report the cross-sectional association between circulating AGE concentrations and insulin secretory function in healthy humans (17\ua0F: 27\ua0M, aged 30\ua0±\ua010\ua0years) with a wide range of BMI (24.6-31.0\ua0kg/m2). Higher circulating concentrations of AGEs were related to increased first phase insulin secretion during IVGTT (r\ua0=\ua00.43; p\ua

Correction to: Pioglitazone reduces cold-induced brown fat glucose uptake despite induction of browning in cultured human adipocytes: a randomised, controlled trial in humans (Diabetologia, 10.1007/s00125-017-4479-9)

The baseline insulin data given in Table 1 for the placebo group were incorrectly reported as 51 ± 10\ua0pmol/l instead of 48 ± 10\ua0pmol/l. This mistake also impacts on data reported in Table 4. The authors also note an error in the reported change in noradrenaline levels, from pre- to post-pioglitazone treatment (Table 4). The relevant rows from Tables 1 and 4 are reproduced here, with corrected data shown in bold. These corrections do not change the statistical significance of any comparison. (Table presented.)