The effect of exercise intensity on circulating hepatokine concentrations in healthy men [Abstract]

The effect of exercise intensity on circulating hepatokine concentrations in healthy men [Abstract

24 h severe energy restriction impairs post-prandial glycaemic control in young, lean males

Intermittent energy restriction (IER) involves short periods of severe energy restriction interspersed with periods of adequate energy intake, and can induce weight loss. Insulin sensitivity is impaired by short-term, complete energy restriction, but the effects of IER are not well known. In randomised order, 14 lean men (age: 25 (SD 4) y; BMI: 24 (SD 2) kg·m-2; body fat: 17 (4) %) consumed 24 h diets providing 100% (10441 (SD 812) kJ; EB) or 25% (2622 (SD 204) kJ; ER) of estimated energy requirements, followed by an oral glucose tolerance test (OGTT; 75g glucose drink) overnight fasted. Plasma/ serum glucose, insulin, non-esterified fatty acids (NEFA), glucagon-like peptide-1 (GLP-1), glucose-dependant insulinotropic peptide (GIP) and fibroblast growth factor-21 (FGF21) were assessed before and after (0 h) each 24 h dietary intervention, and throughout the 2 h OGTT. Homeostatic model assessment of insulin resistance (HOMA2-IR) assessed the fasted response and incremental (iAUC) or total (tAUC) area under the curve were calculated during the OGTT. At 0 h, HOMA2-IR was 23% lower after ER compared to EB (P<0.05). During the OGTT, serum glucose iAUC (P<0.001) serum insulin iAUC (P<0.05) and plasma NEFA tAUC (P<0.01) were greater during ER, but GLP-1 (P=0.161), GIP (P=0.473) and FGF21 (P=0.497) tAUC were similar between trials. These results demonstrate that severe energy restriction acutely impairs postprandial glycaemic control in lean men, despite reducing HOMA2-IR. Chronic intervention studies are required to elucidate the long-term effects of IER on indices of insulin sensitivity, particularly in the absence of weight loss

The influence of adiposity and acute exercise on circulating hepatokines in normal weight and overweight/obese men

Hepatokines are liver-secreted proteins with potential to influence glucose regulation and other metabolic parameters. This study investigated differences in adiposity status on five novel hepatokines and characterised their response to acute moderate-intensity exercise in groups of normal weight and overweight/obese men. Twenty-two men were recruited into normal weight and overweight/obese groups (BMI: 18.5 to 24.9 and 25.0 to 34.9 kg∙m-2). Each completed two experimental trials, exercise and control. During exercise trials, participants performed 60 min of moderate-intensity treadmill exercise (~60% V̇O2 peak) and then rested for 6 h. Participants rested throughout control trials. Circulating fibroblast growth factor-21 (FGF21), follistatin, leukocyte cell-derived chemotaxin 2 (LECT2), fetuin-A and selenoprotein-P (SeP) were measured throughout. Fasted (resting) FGF21 and LECT2 were higher in overweight/obese individuals (129% and 55%; P ≤ 0.01) and correlated with indices of adiposity and insulin resistance; whereas circulating follistatin was lower in overweight/obese individuals throughout trial days (17%, P < 0.05). In both groups, circulating concentrations of FGF21 and follistatin were transiently elevated after exercise for up to 6 h (P ≤ 0.02). Circulating fetuin-A and SeP were no different between groups (P ≥ 0.19) and, along with LECT2, were unaffected by exercise (P ≥ 0.06). These findings show that increased adiposity is associated with a modified hepatokine profile, which may represent a novel mechanism linking excess adiposity to metabolic health. Furthermore, acute perturbations in circulating FGF21 and follistatin after exercise may contribute to the health benefits of an active lifestyle

Acute effects of exercise on appetite, ad libitum energy intake and appetite-regulatory hormones in lean and overweight/obese men and women

BACKGROUND: Acute exercise does not elicit compensatory changes in appetite parameters in lean individuals; however, less is known about responses in overweight individuals. This study compared the acute effects of moderate-intensity exercise on appetite, energy intake and appetite-regulatory hormones in lean and overweight/obese individuals. METHODS: Forty-seven healthy lean (n=22, 11 females; mean(s.d.) 37.5(15.2) years; 22.4(1.5) kg·m−2) and overweight/obese (n=25, 11 females; 45.0(12.4) years, 29.2(2.9) kg·m−2) individuals completed two, 8-h trials (exercise and control). In the exercise trial, participants completed 60 min treadmill exercise (59(4)% peak oxygen uptake) at 0–1 h and rested thereafter whilst participants rested throughout the control trial. Appetite ratings and concentrations of acylated ghrelin, peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) were measured at pre-determined intervals. Standardised meals were consumed at 1.5 and 4 h and an ad libitum buffet meal was provided at 7 h. RESULTS: Exercise suppressed appetite (95% CI −3.1 to −0.5 mm, P=0.01), and elevated delta PYY (95% CI 10 to 17 pg·ml−1, P<0.001) and GLP-1 (95% CI 7 to 10 pmol·l−1, P<0.001) concentrations. Delta acylated ghrelin concentrations (95% CI −4.6 to 3.4 pg·ml−1, P=0.76) and ad libitum energy intake (95% CI −391 to 346 kJ, P=0.90) were similar between trials. Subjective and hormonal appetite parameters and ad libitum energy intake were similar between lean and overweight/obese individuals (Pgreater than or equal to0.27). The exercise-induced elevation in delta GLP-1 was greater in overweight/obese individuals (trial-by-group interaction P=0.01), whereas lean individuals exhibited a greater exercise-induced increase in delta PYY (trial-by-group interaction P<0.001). CONCLUSIONS: Acute moderate-intensity exercise transiently suppressed appetite and increased PYY and GLP-1 in the hours after exercise without stimulating compensatory changes in appetite in lean or overweight/obese individuals. These findings underscore the ability of exercise to induce a short-term energy deficit without any compensatory effects on appetite regardless of weight status

The effects of sprint interval exercise training on hepatic and peripheral insulin sensitivity (IS), as well as intrahepatic triglyceride (IHTG), in men with nonalcoholic fatty liver disease (NAFLD) [Abstract]

The effects of sprint interval exercise training on hepatic and peripheral insulin sensitivity (IS), as well as intrahepatic triglyceride (IHTG), in men with nonalcoholic fatty liver disease (NAFLD) [Abstract

Physical activity is inversely associated with hepatic fibro-inflammation: a population-based cohort study using UK Biobank Data

Background & aims:  Physical activity (PA) is recommended in the management of non-alcoholic fatty liver disease (NAFLD) given beneficial effects on liver fat and cardiometabolic risk. Using data from the UK Biobank population-cohort, this study examined associations between habitual PA and hepatic fibro-inflammation.  Methods:  840 men and women aged 55-70 years were included in this cross-sectional study. Hepatic fibro-inflammation (iron-corrected T1 [cT1]) and liver fat were measured using MRI, whilst body fat was measured using dual-energy X-ray absorptiometry. PA was measured using accelerometry. Generalised linear models examined associations between PA (light [LPA], moderate [MPA], vigorous [VPA], moderate-to-vigorous [MVPA] and mean acceleration) and hepatic cT1. Models were fitted for the whole sample and separately for upper and lower median groups for body and liver fat. Models were adjusted for sociodemographic and lifestyle variables.  Results:  In the full sample, LPA (-0.08 ms [-0.12 to -0.03]), MPA, (-0.13 ms [-0.21 to -0.05]), VPA (-1.16 ms [-1.81 to -0.51]), MVPA (-0.14 ms (-0.21 to -0.06]) and mean acceleration (-0.67 ms [-1.05 to-0.28]) were inversely associated with hepatic cT1. With the sample split by median liver or body fat, only VPA was inversely associated with hepatic cT1 in the upper-median groups for body (-2.68 ms [-4.24 to -1.13]) and liver fat (-2.33 [-3.73 to -0.93]). PA was unrelated to hepatic cT1 in the lower-median groups.  Conclusions:  Within a population-based cohort, device-measured PA is inversely associated with hepatic fibro-inflammation. This relationship is strongest with VPA and is greater in people with higher levels of body and liver fat.</p

Impact of impaired glucose regulation on hepatic and systemic inflammation in men with non-alcoholic fatty liver disease [Abstract]

Impact of impaired glucose regulation on hepatic and systemic inflammation in men with non-alcoholic fatty liver disease [Abstract]</p