Mika Venojärvi

Association of ADIPOQ gene variants with body weight, type 2 diabetes and serum adiponectin concentrations: the Finnish Diabetes Prevention Study

BackgroundAdiponectin, secreted mainly by mature adipocytes, is a protein with insulin-sensitising and anti-atherogenic effects. Human adiponectin is encoded by the ADIPOQ gene on the chromosomal locus 3q27. Variations in ADIPOQ are associated with obesity, type 2 diabetes (T2DM) and related phenotypes in several populations. Our aim was to study the association of the ADIPOQ variations with body weight, serum adiponectin concentrations and conversion to T2DM in overweight subjects with impaired glucose tolerance. Moreover, we investigated whether ADIPOQ gene variants modify the effect of lifestyle changes on these traits.MethodsParticipants in the Finnish Diabetes Prevention Study were randomly assigned to a lifestyle intervention group or a control group. Those whose DNA was available (n = 507) were genotyped for ten ADIPOQ single nucleotide polymorphisms (SNPs). Associations between SNPs and baseline body weight and serum adiponectin concentrations were analysed using the univariate analysis of variance. The 4-year longitudinal weight data were analysed using linear mixed models analysis and the change in serum adiponectin from baseline to year four was analysed using Kruskal-Wallis test. In addition, the association of SNPs with the risk of developing T2DM during the follow-up of 0-11 (mean 6.34) years was analysed by Cox regression analysis.Resultsrs266729, rs16861205, rs1501299, rs3821799 and rs6773957 associated significantly (p < 0.05) with body weight at baseline and in the longitudinal analyses. The rs266729 C allele and the rare minor alleles of rs2241766 and rs2082940 were associated with an increased adjusted hazard ratio of developing T2DM. The differences in baseline serum adiponectin concentrations were seen according to rs16861210, rs17366568, rs2241766, rs6773957 and rs2082940 and differences in the change of serum adiponectin levels from baseline to the four year examination were seen according to rs16861205, especially in subjects who were able to lose weight during the first year of intervention.ConclusionsThese results from the Finnish Diabetes Prevention Study support the concept that genetic variation in ADIPOQ locus contributes to variation in body size and serum adiponectin concentrations and may also modify the risk of developing T2DM.Trial registration numberClinicalTrials.gov NCT00518167

Nordic walking decreased circulating chemerin and leptin concentrations in middle-aged men with impaired glucose regulation

Abstract Background. Dysfunction of adipose tissue is one of the major factors leading to insulin resistance. Altered adipokine concentration is an early sign of adipose tissue dysfunction. The aim of this study was to assess the impact of exercise intervention on adipokine profile, glycemic control, and risk factors of the metabolic syndrome (MeS) in men with impaired glucose regulation (IGR). Methods. Overweight and obese men with IGR (n =144) aged 40–65 years were studied at baseline and at 12 weeks in a randomized controlled multicenter intervention study. BMI varied from 25.1 to 34.9. The subjects were randomized into one of three groups: 1) a control group (C; n =47), 2) a Nordic walking group (NW; n =48), or 3) a resistance training group (RT; n =49). Results. Leptin concentrations decreased in the NW group compared to both other groups. Both types of exercise intervention significantly decreased serum chemerin concentrations compared to the C group. In the NW group also body fat percentage, fatty liver index (FLI), and total and LDL cholesterol concentrations decreased compared to the RT group. Conclusions. Nordic walking intervention seems to decrease chemerin and leptin levels, and subjects in this intervention group achieved the most beneficial effects on components of MeS.

Sleep of professional athletes: Underexploited potential to improve health and performance

ABSTRACT Sleep disorders have become increasingly prevalent affecting health and working ability. Restorative sleep may be considered important for athletes’ successful recovery and performance. However, some athletes seem to experience major problems in sleeping. Thus far, there is limited scientific information about their sleep. This study aimed to evaluate the quality of sleep and the prevalence of sleep disorders as well as the impact of a structured sleep counselling protocol in professional athletes. A total of 107 professional ice hockey players participated in the study. The exploratory observational 1-year follow-up study consisted of questionnaire-based sleep assessment followed by general sleep counselling and, when needed, polysomnography and an individual treatment plan. One in every four players was found to have a significant problem in sleeping. All athletes considered sleep essential for their health and three in every four players considered that counselling would improve their performance. Counselling and individual treatment were found to improve significantly the quality of sleep with the mean alteration of 0.6 (95% CI 0.2–1.0, P = 0.004) in a scale from 0 to 10. Our results support that sleep problems are common in professional athletes. However, systematic examination, counselling and individual treatment planning can improve the quality of their sleep.

Unfavorable influence of structured exercise program on total leisure‐time physical activity

In randomized controlled trials (RCTs), with customized structured physical exercise activity (SPEA) interventions, the dose of leisure‐time physical activity (LTPA) should exceed the LTPA dose of the nonexercising control (C) group. This increase is required to substantiate health improvements achievable by exercise. We aimed to compare the dose of SPEA, LTPA, and total LTPA (SPEA + LTPA) between a randomized Nordic walking (NW) group, a power‐type resistance training (RT) group, and a C group during a 12‐week exercise intervention in obese middle‐aged men (n = 144) with impaired glucose regulation. The dose of physical activity was measured with diaries using metabolic equivalents. No significant difference (P > 0.107) between the groups was found in volume of total LTPA. The volume of LTPA was, however, significantly higher (P < 0.050) in the C group than in the NW group, but not compared with the RT group. These results indicate that structured exercise does not automatically increase the total LTPA level, possibly, as a result of compensation of LTPA with structured exercise or spontaneous activation of the C group. Thus, the dose of total LTPA and the possible changes in spontaneous LTPA should be taken into account when implementing a RCT design with exercise intervention.

Unfavorable influence of structured exercise program on total leisure- time physical activity

In randomized controlled trials (RCTs), with customized structured physical exercise activity (SPEA) interventions, the dose of leisure‐time physical activity (LTPA) should exceed the LTPA dose of the nonexercising control (C) group. This increase is required to substantiate health improvements achievable by exercise. We aimed to compare the dose of SPEA, LTPA, and total LTPA (SPEA + LTPA) between a randomized Nordic walking (NW) group, a power‐type resistance training (RT) group, and a C group during a 12‐week exercise intervention in obese middle‐aged men (n = 144) with impaired glucose regulation. The dose of physical activity was measured with diaries using metabolic equivalents. No significant difference (P > 0.107) between the groups was found in volume of total LTPA. The volume of LTPA was, however, significantly higher (P < 0.050) in the C group than in the NW group, but not compared with the RT group. These results indicate that structured exercise does not automatically increase the total LTPA level, possibly, as a result of compensation of LTPA with structured exercise or spontaneous activation of the C group. Thus, the dose of total LTPA and the possible changes in spontaneous LTPA should be taken into account when implementing a RCT design with exercise intervention.

Humanin skeletal muscle protein levels increase after resistance training in men with impaired glucose metabolism

Humanin (HN) is a mitochondrially encoded and secreted peptide linked to glucose metabolism and tissue protecting mechanisms. Whether skeletal muscle HN gene or protein expression is influenced by exercise remains unknown. In this intervention study we show, for the first time, that HN protein levels increase in human skeletal muscle following 12 weeks of resistance training in persons with prediabetes. Male subjects (n = 55) with impaired glucose regulation (IGR) were recruited and randomly assigned to resistance training, Nordic walking or a control group. The exercise interventions were performed three times per week for 12 weeks with progressively increased intensity during the intervention period. Biopsies from the vastus lateralis muscle and venous blood samples were taken before and after the intervention. Skeletal muscle and serum protein levels of HN were analyzed as well as skeletal muscle gene expression of the mitochondrially encoded gene MT‐RNR2, containing the open reading frame for HN. To elucidate mitochondrial training adaptation, mtDNA, and nuclear DNA as well as Citrate synthase were measured. Skeletal muscle HN protein levels increased by 35% after 12 weeks of resistance training. No change in humanin protein levels was seen in serum in any of the intervention groups. There was a significant correlation between humanin levels in serum and the improvements in the 2 h glucose loading test in the resistance training group. The increase in HN protein levels in skeletal muscle after regular resistance training in prediabetic males may suggest a role for HN in the regulation of glucose metabolism. Given the preventative effect of exercise on diabetes type 2, the role of HN as a mitochondrially derived peptide and an exercise‐responsive mitokine warrants further investigation.

Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance

In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n = 10) were compared with subjects with impaired glucose tolerance (IGT) (n = 8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P = 0.031) and HSP90 was 380% higher (P < 0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research.

Stress Proteins and Heat Shock Proteins: Role in Muscle Building and Sports Nutrition

The heat shock proteins (HSPs) are a family of proteins contributing to cellular protection, protein homeostasis and cell survival against a variety of environmental and metabolic stresses. HSPs, originally identified as heat-inducible gene products, facilitate cell proliferation and regeneration, protect against tissue injury, repair damaged proteins, assist in protein refolding, protect proteins against aggregation and maintain overall integrity of cellular components. A continuous interplay between mechanisms that drive protein synthesis and those that boost protein degradation is an important regulating factor of skeletal muscle mass, where HSPs may play an important role. Both acute and chronic exercise induce HSP expression. As a physiological tool, physical exercise can be considered the safest strategy to enhance skeletal muscle HSP levels. Studies on the modulation of skeletal muscle HSP levels using antioxidant and dietary supplementation strategies gave contradictory results, and this line of research deserves greater effort.

Prenatal and Childhood Growth, Chemerin Concentrations, and Metabolic Health in Adult Life

Several noncommunicable diseases have their origins in early developmental phases. One factor possibly explaining the association between early growth and later health could be adipocyte function. The objective of this study was to assess the association between the adipocytokine chemerin and early growth and later health. 1074 participants from Helsinki Birth Cohort Study born 1934–1944 with information on prenatal and childhood growth participated. Metabolic outcomes include glucose tolerance, adiposity, and chemerin concentration. Mean chemerin concentrations were 5.0 ng/mL higher in women than in men (95% CI 2.7 to 7.2, p < 0.001). The strongest correlate of chemerin concentration was adult waist circumference and body fat percentage (r = 0.22, p < 0.001 and r = 0.21, p < 0.001, resp.). After adjustment for body fat percentage, chemerin concentration was 5.4 ng/mL lower in subjects with type 2 diabetes than in those with normal glucose tolerance (−0.2 to 10.9, p = 0.06). It was 3.0 ng/mL higher in those with metabolic syndrome than in those without (0.6 to 5.3, p = 0.01). No measure of early growth was associated with chemerin concentration. Our findings do not support a role for chemerin in linking early growth with later metabolic health.

Plasma irisin is increased following 12 weeks of Nordic walking and associates with glucose homoeostasis in overweight/obese men with impaired glucose regulation

Abstract Irisin is a myokine that is thought to be secreted in response to exercise that may help to prevent obesity and maintain normal glucose metabolism. In this study we investigated the associations between irisin and glucose homeostasis in middle-aged, overweight and obese men (n =  144) with impaired glucose regulation, and the impact of exercise training on these relationships. The participants underwent 12 weeks of resistance or aerobic (Nordic walking) exercise training three times per week, 60 minutes per session. Venous blood (n = 105) and skeletal muscle samples (n = 45) were obtained at baseline and post-intervention. Compared to controls, Nordic walking, but not resistance training, increased irisin levels in plasma (9.6 ± 4.2%, P = 0.014; 8.7 ±  4.9%, P = 0.087; respectively) compared to controls. When considering all subjects, baseline irisin correlated positively with atherogenic index of plasma (r = 0.244, P = 0.013) and 2-hour insulin levels (r = 0.214, P = 0.028), and negatively with age (r = −0.262, P = 0.007), adiponectin (r = −0.240, P = 0.014) and McAuley index (r = −0.259, P = 0.008). Training-induced FNDC5 mRNA changes were negatively correlated with HbA1c (r = −0.527, P = 0.030) in the resistance training group and with chemerin in the Nordic walking group (r = −0.615, P = 0.033). In conclusion, 12-weeks of Nordic walking was more effective than resistance training in elevating plasma irisin, in middle-aged men with impaired glucose tolerance. Thus, the change in irisin in response to exercise training varied by the type of exercise but showed limited association with improvements in glucose homeostasis.