Excessive daytime napping independently associated with decreased insulin sensitivity in cross-sectional study – Hyogo Sleep Cardio-Autonomic Atherosclerosis cohort study

BackgroundAlthough excessive daytime napping has been shown to be involved in diabetes occurrence, its impact on insulin secretion and sensitivity has not been elucidated. It is speculated that excessive napping disrupts the sleep-wake rhythm and increases sympathetic nerve activity during the day, resulting in decreased insulin sensitivity, which may be a mechanism leading to development of diabetes. We previously conducted a cross-sectional study that showed an association of autonomic dysfunction with decreased insulin sensitivity, though involvement of autonomic function in the association between napping and insulin sensitivity remained unclear. Furthermore, the effects of napping used to supplement to short nighttime sleep on insulin secretion and sensitivity are also unknown. In the present cross-sectional study, we examined the relationships of daytime nap duration and autonomic function with insulin secretion and sensitivity in 436 subjects enrolled in the Hyogo Sleep Cardio-Autonomic Atherosclerosis (HSCAA) Cohort Study who underwent a 75-g oral glucose tolerance test (75-g OGTT), after excluding those already diagnosed with diabetes.MethodsDaytime nap duration was objectively measured using actigraphy, with the subjects divided into the short (≤1 hour) and long (>1 hour) nap groups. Insulin secretion and sensitivity were determined using 75-g OGTT findings. Standard deviation of normal to normal R-R interval (SDNN), a measure of autonomic function, was also determined based on heart rate variability. Subgroup analysis was performed for the associations of napping with insulin secretion and sensitivity, with the results stratified by nighttime sleep duration of less or greater than six hours.ResultsSubjects in the long nap group exhibited lower insulin sensitivity parameters (QUICKI: β=-0.135, p<0.01; Matsuda index: β=-0.119, p<0.05) independent of other clinical factors. In contrast, no associations with insulin secretion were found in either group. Furthermore, the association of long nap duration with insulin sensitivity was not confounded by SDNN. Specific subgroup analyses revealed more prominent associations of long nap habit with lower insulin sensitivity in subjects with a short nighttime sleep time (β=-0.137, p<0.05).ConclusionLong daytime nap duration may be a potential risk factor for decreased insulin sensitivity

Global legume diversity assessment : concepts, key indicators, and strategies

While many plant species are considered threatened under anthropogenic pressure, it remains uncertain how rapidly we are losing plant species diversity. To fill this gap, we propose a Global Legume Diversity Assessment (GLDA) as the first step of a global plant diversity assessment. Here we describe the concept of GLDA and its feasibility by reviewing relevant approaches and data availability. We conclude that Fabaceae is a good proxy for overall angiosperm diversity in many habitats and that much relevant data for GLDA are available. As indicators of states, we propose comparison of species richness with phylogenetic and functional diversity to obtain an integrated picture of diversity. As indicators of trends, species loss rate and extinction risks should be assessed. Specimen records and plot data provide key resources for assessing legume diversity at a global scale, and distribution modeling based on these records provide key methods for assessing states and trends of legume diversity. GLDA has started in Asia, and we call for a truly global legume diversity assessment by wider geographic collaborations among various scientists.This paper is an outcome of the workshop on the global legume diversity assessment held from 19 to 22 August 2011 in Kyushu University, Japan.The Environment Research and Technology Development Fund (S9) of the Ministry of the Environment, Japan and the JSPS fund for Global Center of Excellence Program “Asian Conservation Ecology”.http://www.botanik.univie.ac.at/iapt/s_taxon.phpam201

Sleep, Autonomic Nervous Function and Atherosclerosis

Behavioral and psychosocial factors related to development of cardiovascular disease have been gaining increased attention. Notably, sleep is considered to be one of the most important behavioral factors involved in progression of atherosclerosis and cardiovascular events, with autonomic nervous function a potential mechanism. Several studies have shown associations of sleep and autonomic dysfunction with major surrogate markers of atherosclerosis, such as carotid intima-media thickness and arterial stiffness. Endocrinological, immunological, oxidative, inflammatory, and metabolic responses, as well as endothelial dysfunction may mediate the effects of the autonomic nervous system. For this review, we examined recent findings related to sleep, autonomic nervous dysfunction, and atherosclerosis, with the aim of understanding the involved pathophysiological mechanisms

Cardiac Hypertrophy and Related Dysfunctions in Cushing Syndrome Patients—Literature Review

The survival rate of adrenal Cushing syndrome patients has been greatly increased because of the availability of appropriate surgical and pharmacological treatments. Nevertheless, increased possibility of a heart attack induced by a cardiovascular event remains a major risk factor for the survival of affected patients. In experimental studies, hypercortisolemia has been found to cause cardiomyocyte hypertrophy via glucocorticoid receptor activation, including the possibility of cross talk among several hypertrophy signals related to cardiomyocytes and tissue-dependent regulation of 11β-hydroxysteroid dehydrogenase type 1. However, the factors are more complex in clinical cases, as both geometric and functional impairments leading to heart failure have been revealed, and their associations with a wide range of factors such as hypertension are crucial. In addition, knowledge regarding such alterations in autonomous cortisol secretion, which has a high risk of leading to heart attack as well as overt Cushing syndrome, is quite limited. When considering the effects of treatment, partial improvement of structural alterations is expected, while functional disorders are controversial. Therefore, whether the normalization of excess cortisol attenuates the risk related to cardiac hypertrophy has yet to be fully elucidated

A role for galectin-1 in the immune response to peripheral nerve injury.

International audienceGalectin-1 (Gal1) is a multi-functional protein that has key roles in organismal growth and survival. In the adult nervous system, Gal1 promotes axonal regeneration following peripheral nerve injury. Although the mechanism by which Gal1 promotes regeneration is unclear, previous reports suggested that Gal1 acts indirectly by activating macrophages. An appropriate response of macrophages is crucial for repair of injured nerves: these immune cells remove obstructive axon and myelin debris in the distal nerve. Here we establish a role for Gal1 in the accumulation of immune cells following peripheral axotomy. We used immunohistochemistry to visualize macrophages (F4/80) in wild-type (Lgals1(+/+)) and knockout (Lgals1(-/-)) mouse sciatic nerves following injury and/or manipulation of Gal1 levels. Density of F4/80 immunoreactivity, which peaks around 3 days post-injury, was decreased in Lgals1(+/+) nerves injected with Gal1 antibody. The typical injury-induced peak of macrophage/microglial density was delayed in the sciatic nerves and fifth lumbar dorsal root ganglia of Lgals1(-/-) mice relative to control mice. Injection of oxidized Gal1 into uninjured sciatic nerve promoted the accumulation of macrophages in Lgals1(+/+) nerves. Finally, we used transplants of sciatic nerve to uncover a compensatory mechanism in Lgals1(-/-) mice that allows for macrophage accumulation (albeit delayed and diminished) following axotomy. We conclude that Gal1 is necessary to direct the typical accumulation of macrophages in the injured peripheral nerve, and that Gal1 is sufficient to promote macrophage accumulation in the uninjured nerve of wild-type mice

fosB Grene Products Trigger Cell Proliferation and Morphological Alteration with an Increased Expression of a Novel Processed Form of Galectin-1 in the Rat 3Y1 Embryo Cell Line

In this study, we established rat 3Y1 embryo cell lines expressing FosB and AFosB as fusion proteins (ER-FosB, ER-AFosB) with the ligand-binding domain of human estrogen receptor (ER). The binding of estrogen to the fusion proteins resulted in their nuclear translocation. After estrogen administration, exponentially growing cells expressing ERAFosB, and to a lesser extent ER-FosB, underwent morphological alteration from the flat fibroblastic shape to an extended bipolar shape, and ceased proliferating. Such morphological alteration was also induced in quiescent cells expressing ER-AFosB and ER-FosB after one round of cell division triggered by estrogen administration. The cells expressing ER-AFosB changed shape frequently, and the content of F-actin in the cytoplasm detected by binding of Alexa 488-phalloidin significantly decreased after the morphological alteration. By two-dimensional gel electrophoresis analysis of cellular proteins from the cells expressing ER-AFosB, we identified several proteins whose expression either increased or decreased after estrogen administration. Two of these proteins were identified from their amino acid sequences as novel processed form of galectin-1