Nucleobindin-2 (NUCB2)-derived nesfatin-1 located in the brain has been implicated in the satiety and control of energy metabolism. Nesfatin-1 is also produced in the periphery and present in the ...plasma. It has recently been reported that NUCB2/nesfatin-1 is localized in pancreatic islet β-cells in mice and rats and released from islets. However, its function in islets remains largely unknown. This study examined direct effects of nesfatin-1 on insulin release from pancreatic islets and on cytosolic Ca2+ concentration (Ca2+i) in single β-cells from ICR mice. In the presence of 8.3 mmol/L glucose, nesfatin-1 at 10-10-10-9 mol/L tended to increase and at 10-8 mol/L increased insulin release from isolated islets, while at 2.8 mmol/L glucose nesfatin-1 had no effect. Furthermore, nesfatin-1 at 10-10-10-8 mol/L increased Ca2+i in single β-cells in the presence of 8.3 but not 2.8 mmol/L glucose. The nesfatin-1-induced Ca2+i increase and insulin release were inhibited by removal of extracellular Ca2+ and by addition of nitrendipine, a blocker of voltage-dependent L-type Ca2+ channels. Unexpectedly, the Ca2+i responses to nesfatin-1 were unaltered by inhibitors of protein kinase A (PKA) and phospholipase A2 (PLA2). These results indicate that nesfain-1 potentiates glucose-induced insulin secretion by promoting Ca2+ influx through L-type Ca2+ channels independently of PKA and PLA2 in mouse islet β-cells.
Abstract Consumption of high-fat diet (HFD) induces energy imbalance and consequently obesity. In the pathogenesis of obesity, HFD triggers inflammation in the hypothalamus including arcuate nucleus ...(ARC). Interleukin-10 (IL-10) is a representative anti-inflammatory cytokine, known to ameliorate the adipose tissue inflammation and insulin resistance in obesity. However, the effect of IL-10 on the hypothalamic inflammation remains less defined. We here report the effect of over-expression of murine IL-10 using adeno-associated virus (AAV) vector on the inflammation in ARC and feeding behavior in HFD-induced obese (DIO) mice. DIO mice exhibited reduced POMC expression and elevated IKKs (IκB kinases) and SOCS3 expression in ARC. Overexpression of mIL-10 using AAV vector ameliorated obesity in parallel with restoration of ARC POMC expression in DIO mice. Moreover, IL-10 treatment suppressed IKKs activation and SOCS3 expression in ARC of DIO mice. These results suggest that IL-10 gene transfer provides an effective approach for counteracting HFD-induced inflammation and leptin resistance in ARC to prevent progression of obesity.
Abstract. Purpose The initial cardiopulmonary response to exercise is hypothesized to be a useful predictor of aerobic threshold in patients with heart failure. This study aimed to evaluate the ...correlation between aerobic threshold and cardiopulmonary responses to exercise onset by comparing patients with heart failure using preserved (>- 50%) and reduced (< 50%) left ventricular ejection fractions. Participants and Methods Twenty-eight males (age, 36-82 years; 12 with preserved and 16 with reduced left ventricular ejection fractions) underwent a progressive submaximal cardiopulmonary exercise test using a cycle ergometer. The aerobic threshold, time constant, and area under the oxygen uptake curve for the first 4 min (VO2AUC) were determined. Results A significant association was observed between aerobic threshold and VO2AUC in the reduced group but not in the preserved group. No significant correlations were found between time constant and VO2AUC or between aerobic threshold and time constant in either group. Conclusion The results suggest that VO2AUC measured from exercise onset to an initial 4-min period could provide an easily and safely obtained predictor to assess aerobic capacity in people with reduced left ventricular ejection fractions.
Purpose The initial cardiopulmonary response to exercise is hypothesized to be a useful predictor of aerobic threshold in patients with heart failure. This study aimed to evaluate the correlation ...between aerobic threshold and cardiopulmonary responses to exercise onset by comparing patients with heart failure using preserved (≥50%) and reduced (<50%) left ventricular ejection fractions. Participants and Methods Twenty-eight males (age, 36–82 years; 12 with preserved and 16 with reduced left ventricular ejection fractions) underwent a progressive submaximal cardiopulmonary exercise test using a cycle ergometer. The aerobic threshold, time constant, and area under the oxygen uptake curve for the first 4 min (V̇O2AUC) were determined. Results A significant association was observed between aerobic threshold and V̇O2AUC in the reduced group but not in the preserved group. No significant correlations were found between time constant and V̇O2AUC or between aerobic threshold and time constant in either group. Conclusion The results suggest that V̇O2AUC measured from exercise onset to an initial 4-min period could provide an easily and safely obtained predictor to assess aerobic capacity in people with reduced left ventricular ejection fractions.
Nucleobindin-2 (NUCB2)-derived nesfatin-1 located in the brain has been implicated in the satiety and control of energy metabolism. Nesfatin-1 is also produced in the periphery and present in the ...plasma. It has recently been reported that NUCB2/nesfatin-1 is localized in pancreatic islet β-cells in mice and rats and released from islets. However, its function in islets remains largely unknown. This study examined direct effects of nesfatin-1 on insulin release from pancreatic islets and on cytosolic Ca(2+) concentration (Ca(2+)(i)) in single β-cells from ICR mice. In the presence of 8.3 mmol/L glucose, nesfatin-1 at 10(-10)-10(-9) mol/L tended to increase and at 10(-8) mol/L increased insulin release from isolated islets, while at 2.8 mmol/L glucose nesfatin-1 had no effect. Furthermore, nesfatin-1 at 10(-10)-10(-8) mol/L increased Ca(2+)(i) in single β-cells in the presence of 8.3 but not 2.8 mmol/L glucose. The nesfatin-1-induced Ca(2+)(i) increase and insulin release were inhibited by removal of extracellular Ca(2+) and by addition of nitrendipine, a blocker of voltage-dependent L-type Ca(2+) channels. Unexpectedly, the Ca(2+)(i) responses to nesfatin-1 were unaltered by inhibitors of protein kinase A (PKA) and phospholipase A(2) (PLA(2)). These results indicate that nesfain-1 potentiates glucose-induced insulin secretion by promoting Ca(2+) influx through L-type Ca(2+) channels independently of PKA and PLA(2) in mouse islet β-cells.
Objectives
To evaluate the impact of Facial radiance or Glow on the perception of age (PA) and to assess which facial signs most influence PA.
Material and Methods
The faces of 1058 differently aged ...women (18‐80 years) of six different ethnicities/countries (China, Japan, Korea, India, South Africa, and Brazil) were photographed under standard conditions. These allowed to focus on 20 different facial signs that were further graded by experts, using referential Atlases dedicated to facial aging. In each of the six countries, 100 local women were recruited as naïve panels to express their perceptions on Glow and Age on each full‐face photograph (blind coded) of the local studied woman.
Results
A decreased Glow/Radiance appears clearly associated with an increased perceived age in all studied subjects, especially among Chinese, Japanese, and South African women. With regard facial signs, Skin texture (Wrinkles of all kinds), Ptosis/Sagging, and Pigmentation signs prevail in almost all women at the exception of South African women where Pigmentation signs and Cheek skin pores largely predominate in the perception of both Glow and PA. Pigmentation signs are of a very high weight among Chinese and Japanese women.
Conclusion
Despite some collective agreements, the present study shows some specificities within the women of the six ethnicities/countries. PA, a core index of antiaging strategies, goes along with facial Glow in almost all studied women. The duller the facial skin, the older it is perceived.
Purpose: This study aimed to identify the correlation between aerobic threshold（ AT） andcardiopulmonary response at the start of exercise in patients with myocardial infarction（ MI）.Subjects and ...Methods: Thir ty-one male patients with MI underwent a sub-maximalcardiopulmonary exercise test with expiratory gas analysis to determine their peak oxygenuptake （V ・O2） level, using Ramp protocol.Results: The patients demonstrated an extended time constant（ TC） and decline in AT in thisstudy. Extended TC suggested impaired cardiac function due to reduced left ventricularejection fraction （LVEF）, as well as an LVEF of 59.8％ on average. However, there was nosignificant correlation between TC and AT. Pearson product-moment correlation coefficientswere 0.56 between AT and area under the oxygen uptake curve （V ・O2AUC）, –0.22 between TCand V ・O2AUC, and –0.23 between AT and TC.Conclusion: V ・O2AUC is representative of oxygen utilization and is correlated with AT inpatients with MI.
Purpose This study compared cardiorespiratory responses during wheelchair driving under two different conditions of spinal curvature. Subjects Sixteen healthy men who provided their written informed ...consent. Methods We investigated respiratory rate (RR), tidal volume (TV), minute ventilation volume (VE), movements of the thoracic trunk and abdomen at maximal respiration, and heart rate (HR) at rest and during wheelchair driving 20 seconds after the start of driving (phase I), under two spinal curvature conditions. Results RR of wheelchair driving was significantly increased by enhanced spinal curvature, whereas TV and HR during wheelchair driving showed no significant changes. TV and VE were significantly decreased by enhanced spinal curvature in phase 1. In addition, O2 debt was significantly increased by enhanced spinal curvature. Conclusion We conclude that in wheelchair driving, enhanced spinal curvature increases O2 debt, due to reduced TV and VE responses in phase I.
Nucleobindin-2 (NUCB2)-derived nesfatin-1 located in the brain has been implicated in the satiety and control of energy metabolism. Nesfatin-1 is also produced in the periphery and present in the ...plasma. It has recently been reported that NUCB2/nesfatin-1 is localized in pancreatic islet β-cells in mice and rats and released from islets. However, its function in islets remains largely unknown. This study examined direct effects of nesfatin-1 on insulin release from pancreatic islets and on cytosolic Ca2+ concentration (Ca2+i) in single β-cells from ICR mice. In the presence of 8.3 mmol/L glucose, nesfatin-1 at 10-10-10-9 mol/L tended to increase and at 10-8 mol/L increased insulin release from isolated islets, while at 2.8 mmol/L glucose nesfatin-1 had no effect. Furthermore, nesfatin-1 at 10-10-10-8 mol/L increased Ca2+i in single β-cells in the presence of 8.3 but not 2.8 mmol/L glucose. The nesfatin-1-induced Ca2+i increase and insulin release were inhibited by removal of extracellular Ca2+ and by addition of nitrendipine, a blocker of voltage-dependent L-type Ca2+ channels. Unexpectedly, the Ca2+i responses to nesfatin-1 were unaltered by inhibitors of protein kinase A (PKA) and phospholipase A2 (PLA2). These results indicate that nesfain-1 potentiates glucose-induced insulin secretion by promoting Ca2+ influx through L-type Ca2+ channels independently of PKA and PLA2 in mouse islet β-cells.
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