Fibroblast growth factor 21 (FGF21) plays an important role in the regulation of energy homeostasis during starvation and has an excellent therapeutic potential for the treatment of type 2 diabetes in rodents and monkeys. Acute exercise affects glucose and lipid metabolism by increasing glucose uptake and lipolysis. However, it is not known whether acute exercise affects FGF21 expression. Here, we showed that serum FGF21 level is increased in mice after a single bout of acute exercise, and that this is accompanied by increased serum levels of free fatty acid, glycerol and ketone body. FGF21 gene expression was induced in the liver but not in skeletal muscle and white adipose tissue of mice after acute exercise, and further, the gene expression levels of hepatic peroxisome proliferator-activated receptor α (PPARα) and activating transcription factor 4 (ATF4) were also increased. In addition, we observed increased FGF21 level in serum of healthy male volunteers performing a treadmill run at 50 or 80% VO2max. These results suggest that FGF21 may also be associated with exercise-induced lipolysis in addition to increased catecholamines and reduced insulin.

Natives of the tropics are able to tolerate high ambient temperatures. This results from their long-term residence in hot and often humid tropical climates. This study was designed to compare the peripheral mechanisms of thermal sweating in tropical natives with that of their temperate counterparts. Fifty-five healthy male subjects including 20 native Koreans who live in the temperate Korean climate (Temperate-N) and 35 native tropical Malaysian men that have lived all of their lives in Malaysia (Tropical-N) were enrolled in this study after providing written informed consent to participate. Quantitative sudomotor axon reflex testing after iontophoresis (2 mA for 5 min) with 10% acetylcholine (ACh) was used to determine directly activated (DIR) and axon reflex-mediated (AXR) sweating during ACh iontophoresis. The sweat rate, activated sweat gland density, sweat gland output per single gland activated, and oral and skin temperature changes were measured. The sweat onset time of AXR (nicotinic-receptor-mediated) was 56 s shorter in the Temperate-N than in the Tropical-N subjects (P < 0.0001). The nicotinic-receptor-mediated sweating activity AXR (1), and the muscarinic-receptor-mediated sweating activity DIR, in terms of sweat volume, were 103% and 59% higher in the Temperate-N compared to the Tropical-N subjects (P < 0.0001). The Temperate-N group also had a 17.8% (P < 0.0001) higher active sweat gland density, 35.4% higher sweat output per gland, 0.24 degrees C higher resting oral temperature, and 0.62 degrees C higher resting forearm skin temperature compared to the Tropical-N subjects (P < 0.01). ACh iontophoresis did not influence oral temperature, but increased skin temperature near where the ACh was administered, in both groups. These results suggest that suppressed thermal sweating in the Tropical-N subjects was, at least in part, due to suppressed sweat gland sensitivity to ACh through both recruitment of active sweat glands and the sweat gland output per each gland. This physiological trait guarantees a more economical use of body fluids, thus ensuring more efficient protection against heat stress.

Background: End-stage renal disease (ESRD) is a progressive, debilitating, chronic illness requiring nursing and medical interventions. The goal of this study was to explore the level of depression experienced by patients receiving hemodialysis (n = 146), and to compare the symptoms with the quality of life (QoL) between patients that were depressed and those that were not depressed. Methods: For this descriptive, cross-sectional survey, participants aged 18 and above were recruited from three different regions in the Republic of Korea. The level of depression, symptoms and QoL of the participants were measured by questionnaires from October to December 2006. The data was analyzed with descriptive statistics, the χ² and t test using the SPSS WIN 14.0 program. Results: The prevalence of depression (PHQ-9) among the participants was 25.34%. There were more symptoms reported in the depressed group of patients than in those that were not depressed. In addition, the QoL was not as good in the depressed group when compared to patients that were not depressed. Conclusion: Therefore, the evaluation for depression may be an important part of the management of patients with ESRD. Further research is needed to understand the causal relationship between depression and health outcomes.

Sweating has been associated with the exacerbation of atopic dermatitis (AD) in diverse ways. Acetylcholine (ACh)-mediated sweating is known to be attenuated in AD, but its cause remains obscure. To address this issue, the impact of histamine on ACh-induced sweating was evaluated. Sweating was measured by counting the number of active sweat pores by the starch-iodine reaction and dynamic optical coherence tomography; sweat was visualized using two-photon excitation fluorescence microscopy in mice and the quantitative sudomotor axon reflex test in humans. Both histamine receptor antagonists and H1 receptor (H1R)-knockout (KO) mice were used to determine methodological specificity. Histamine demonstrably inhibited ACh-induced sweating in both mice and humans via H1R-mediated signaling. In sweat glands, ACh inactivated glycogen synthase kinase 3β (GSK3β), a kinase involved in endocytosis and secretion, whereas simultaneous stimulation with histamine activated GSK3β. Results of two-photon excitation fluorescence microscopy confirmed the dynamic motion of sweat and sweat glands after ACh treatment, showing that simultaneous stimulation with histamine altered their dynamic properties. These results indicate that histamine inhibits sweat gland secretions by blocking ACh-induced inactivation of GSK3β. Histamine-mediated hypohidrosis might be involved in the mechanism of abnormal skin dryness in patients with AD.

Tropical natives possess heat tolerance due to the ability to off-load endogenous and exogenous heat efficiently using a minimum amount of sweat. On the other hand, exposure of temperate natives to heat results in exaggerated production of sweat, of which part is lost by dripping and, thus, not available for evaporation. How sweating is modified in natives of temperate climate zones by prolonged residence in the tropics is not well-understood. The aim of this study was to investigate possible changes in the peripheral sweating mechanisms. Sweating responses to iontophoretically applied acetylcholine (ACh) were compared between Japanese subjects having either permanently resided in Japan (Japan resident Japanese, JRJ) or having stayed in the tropics for 2 years or longer (Tropics resident Japanese, TRJ). Quantitative sudomotor axon reflex tests by iontophoresis of ACh (10%, 2 mA for 5 min) were applied to determine directly activated (DIR) and axon reflex-mediated sweating during [AXR(1)] and after [AXR(2)] ACh iontophoresis. The sweat onset time of AXR(1) was 0.6 min shorter in JRJ than in TRJ (P<0.0001), and AXR(1) (P<0.0004), AXR(2) (P<0.0001), and DIR (P<0.0001) sweating responses were larger in JRJ than in TRJ. AXR and DIR sweating volumes (P<0.0001) were negatively correlated, and sweat onset times (P<0.0001) were positively correlated with the duration of residence in the tropics (2 to 13 years). The observed attenuation of sweating in TRJ suggests that temperate natives may acquire heat tolerance with improved sweating economy similar to tropical natives after prolonged residence in the tropics.

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The aim of this study was to investigate the expression of cardiac strain and damage in 18 male marathoners with average age of 52.8 ± 5.0 years running at a 308 km ultra-marathon. Blood samples were collected at pre-race, 100 km, 200 km and 308 km check points for the analysis of cardiac muscle injury markers, creatine kinase (CK), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTnI) and cardiac muscle strain marker, N-terminal pro-brain natriuretic peptide (NT-proBNP). The CK levels increased 1127.2 ± 507.9 IU/L, 5133.8 ± 2492.7 IU/L and 4958.4 ± 2087.9 IU/L at 100 km, 200 km and 308 km, respectively, compared to the pre-race levels. The CK-MB levels increased 20.2 ± 11.2 ng/mL, 73.3 ± 35.6 ng/mL and 68.6 ± 42.6 ng/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The CK-MB/CK ratio showed that the CK-MB mass index was within the normal range (<2.5%) at 100 km, 200 km and 308 km. The cTnI levels showed no significant difference in all check points. The NT-proBNP levels increased 146.55 ± 92.7 pg/mL, 167.95 ± 111.9 pg/mL and 241.23 ± 121.2 pg/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The normal CK-MB mass index (<5.0 ng/mL) and the absence of an increase in the cTnI levels during the 308 km ultra-marathon suggested that no myocardial injury despite an elevation in CK-MB. The increase in NT-proBNP levels probably resulted from continuous hemodynamic cardiac stress and represents a transient physiological myocardial protective response.

Recent studies showed that tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), as well as high-sensitive C-reactive protein (hsCRP) levels are predictive factors of cardiovascular risk. However, the effect of cardiac rehabilitation (CR) intervention in coronary artery disease (CAD) patients on these factors is not known. The aim of this study was to evaluate the effects of CR and exercise on hsCRP and inflammatory cytokine levels in patients with CAD after percutaneous coronary intervention (PCI). CAD patients who underwent PCI were divided into a CR and exercise group (CRE, n = 29) or a control group (CON, n = 10). CR and exercise consisted of 6 weeks supervised exercise training and 8 weeks home-based, self-managed exercise. Compared to pre-experimental levels, TNF-alpha (by 20.4%; p = 0.006) and IL-6 (by 49.0%; p < 0.0001), as well as hsCRP (by 59.4%; p < 0.0001), were markedly decreased after CR and exercise in CAD patients but not in control group, except for IL-6 (by 41.6%; p = 0.001). However, there was no significant alteration of adiposity-related variables such as BMI, percent body fat, and waist circumferences, in both groups. We suggest that CR and exercise in CAD patients after PCI induce significant reduction in hsCRP and inflammatory cytokines (TNF-alpha and IL-6), and marked increase in exercise tolerance and capacity.