Nutrition in aneurysm clipping

Aneurysmal subarachnoid hemorrhage (SAH) is a serious clinical event associated with high mortality and, among survivors, serious morbidity. Maintaining the muscle volume in SAH patients is essential, as rehabilitation is often required after intensive care. In this study, we investigated whether proper nutritional administration improved clinical outcomes based on patients laboratory data and level of activities of daily living. This retrospective study was carried out on 250 consecutive SAH patients who underwent craniotomy within 72 hours of onset from February 2005 to June 2018. Finally, 75 patients with a BMI < 22 kg / m2 were included. We compared postoperative energy and protein intake in relation to measures of biochemical parameters and modified Rankin Scale at discharge. Serum Alb concentrations at 25-35 hospital days was significantly improved by postoperative energy intake of ≥ 25 kcal / kg and protein intake of ≥ 0.8 g / kg per day beginning 3 days. High serum Alb concentrations at 25-35 hospital days following the start of this intake were independent factors for good prognosis. This study suggests that the minimum postoperative nutritional intake per day for SAH patients undergoing aneurysmal clipping is 25 kcal / kg of energy and 0.8 g / kg of protein. Higher serum Alb concentrations corresponded to improved long-term functional outcome

Intestinal epithelial cell-derived IL-15 determines local maintenance and maturation of intraepithelial lymphocytes in the intestine

Interleukin-15 (IL-15) is a cytokine critical for maintenance of intestinal intraepithelial lymphocytes (IELs), especially CD8αα+ IELs (CD8αα IELs). In the intestine, IL-15 is produced by intestinal epithelial cells (IECs), blood vascular endothelial cells (BECs) and hematopoietic cells. However, the precise role of intestinal IL-15 on IELs is still unknown. To address the question, we generated two kinds of IL-15 conditional knockout (IL-15cKO) mice: villin-Cre (Vil-Cre) and Tie2-Cre IL-15cKO mice. IEC-derived IL-15 was specifically deleted in Vil-Cre IL-15cKO mice, whereas IL-15 produced by BECs and hematopoietic cells is deleted in Tie2-Cre IL-15cKO mice. The cell number and frequency of CD8αα IELs and NK IELs were significantly reduced in Vil-Cre IL-15cKO mice. By contrast, CD8αα IELs were unchanged in Tie2-Cre IL-15cKO mice, indicating that IL-15 produced by BECs and hematopoietic cells is dispensable for CD8αα IELs. Expression of an anti-apoptotic factor, Bcl-2, was decreased, whereas Fas expression was increased in CD8αα IELs of Vil-Cre IL-15cKO mice. Forced expression of Bcl-2 by a Bcl-2 transgene partially restored CD8αα IELs in Vil-Cre IL-15cKO mice, suggesting that some IL-15 signal other than Bcl-2 is required for maintenance of CD8αα IELs. Furthermore, granzyme B production was reduced, whereas PD-1 expression was increased in CD8αα IELs of Vil-Cre IL-15cKO mice. These results collectively suggested that IEC-derived IL-15 is essential for homeostasis of IELs by promoting their survival and functional maturation

Deficient of a Clock Gene, Brain and Muscle Arnt-Like Protein-1 (BMAL1), Induces Dyslipidemia and Ectopic Fat Formation

A link between circadian rhythm and metabolism has long been discussed. Circadian rhythm is controlled by positive and negative transcriptional and translational feedback loops composed of several clock genes. Among clock genes, the brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor output cycles kaput (CLOCK) play important roles in the regulation of the positive rhythmic transcription. In addition to control of circadian rhythm, we have previously shown that BMAL1 regulates adipogenesis. In metabolic syndrome patients, the function of BMAL1 is dysregulated in visceral adipose tissue. In addition, analysis of SNPs has revealed that BMAL1 is associated with susceptibility to hypertension and type II diabetes. Furthermore, the significant roles of BMAL1 in pancreatic β cells proliferation and maturation were recently reported. These results suggest that BMAL1 regulates energy homeostasis. Therefore, in this study, we examined whether loss of BMAL1 function is capable of inducing metabolic syndrome. Deficient of the Bmal1 gene in mice resulted in elevation of the respiratory quotient value, indicating that BMAL1 is involved in the utilization of fat as an energy source. Indeed, lack of Bmal1 reduced the capacity of fat storage in adipose tissue, resulting in an increase in the levels of circulating fatty acids, including triglycerides, free fatty acids, and cholesterol. Elevation of the circulating fatty acids level induced the formation of ectopic fat in the liver and skeletal muscle in Bmal1 -/- mice. Interestingly, ectopic fat formation was not observed in tissue-specific (liver or skeletal muscle) Bmal1 -/- mice even under high fat diet feeding condition. Therefore, we were led to conclude that BMAL1 is a crucial factor in the regulation of energy homeostasis, and disorders of the functions of BMAL1 lead to the development of metabolic syndrome

Effect and factors associated with weight and waist circumference reductions in information and communication technology-based specific health guidance

Objectives: Specific health guidance (SHG) has served as a preventive intervention for metabolic syndrome in Japan since 2008. For SHG, health professionals guide diet and physical activity to achieve body weight (BW) and waist circumference (WC) reductions. Since 2013, SHG intervention using information and communication technology (ICT-based SHG) has also been available. Therefore, in this study, we examined the effects of ICT-based SHG, and identified factors associated with BW and WC reductions in response to this intervention. Methods: Our intervention was performed using a smartphone application with videophone guidance and message exchanges provided by health professionals. We analysed 1,994 participants. Primary outcomes included changes in BW and WC after versus before the intervention. We used multiple linear regression analyses to identify factors associated with reductions in BW and WC due to the intervention. Results: The mean ages were 49.3 (standard deviation [SD], 5.8) years for males and 50.5 (SD, 5.8) years for females. The mean BW change was −1.37 kg for both sexes. The mean WC changes were −1.05 for males and −2.05 cm for females. For males, baseline body mass index, pre-intervention action history, and the numbers of videophone communications and messages were significantly associated with larger changes in BW and WC. For females, no factors were significant for BW reduction, while baseline WC and pre-intervention action history were associated with WC reduction. Conclusions: ICT-based SHG reduces BW and WC. Videophone communication and messaging are associated with reductions in BW and WC in males. These results may help to improve the efficacy of ICT-based SHG

Delayed dinnertime impairs glucose tolerance in healthy young adults

Abstract To explore the relationship between mealtime delays of up to 3 h and subsequent glucose fluctuations, healthy young adults were allocated to three delayed dinnertimes in randomized order. Participants consumed test meals for lunch and dinner. After assessing the glucose responses using intermittently scanned continuous glucose monitoring devices (isCGM), the peak glucose elevation, and incremental area under the curve (iAUC) of postprandial glucose during certain intervals increased significantly when the time between lunch and dinner was delayed by 1 h or more. Our results support the importance of improving irregular mealtime habits, such as late eating

Green tea extracts ameliorate high-fat diet-induced muscle atrophy in senescence-accelerated mouse prone-8 mice.

Muscle atrophy (loss of skeletal muscle mass) causes progressive deterioration of skeletal function. Recently, excessive intake of fats was suggested to induce insulin resistance, followed by muscle atrophy. Green tea extracts (GTEs), which contain polyphenols such as epigallocatechin gallate, have beneficial effects on obesity, hyperglycemia, and insulin resistance, but their effects against muscle atrophy are still unclear. Here, we found that GTEs prevented high-fat (HF) diet-induced muscle weight loss in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, an HF diet, or HF with 0.5% GTEs (HFGT) diet for 4 months. The HF diet induced muscle weight loss with aging (measured as quadriceps muscle weight), whereas GTEs prevented this loss. In HF diet-fed mice, blood glucose and plasma insulin concentrations increased in comparison with the control group, and these mice had insulin resistance as determined by homeostasis model assessment of insulin resistance (HOMA-IR). In these mice, serum concentrations of leukocyte cell-derived chemotaxin 2 (LECT2), which is known to induce insulin resistance in skeletal muscle, were elevated, and insulin signaling in muscle, as determined by the phosphorylation levels of Akt and p70 S6 kinases, tended to be decreased. In HFGT diet-fed mice, these signs of insulin resistance and elevation of serum LECT2 were not observed. Although our study did not directly show the effect of serum LECT2 on muscle weight, insulin resistance examined using HOMA-IR indicated an intervention effect of serum LECT2 on muscle weight, as revealed by partial correlation analysis. Accordingly, GTEs might have beneficial effects on age-related and HF diet-induced muscle weight loss, which correlates with insulin resistance and is accompanied by a change in serum LECT2

Green Tea Extracts Attenuate Brain Dysfunction in High-Fat-Diet-Fed SAMP8 Mice

Unhealthy diet promotes progression of metabolic disorders and brain dysfunction with aging. Green tea extracts (GTEs) have various beneficial effects and alleviate metabolic disorders. GTEs have neuroprotective effects in rodent models, but their effects against brain dysfunction in models of aging fed unhealthy diets are still unclear. Here, we showed that GTEs attenuate high-fat (HF) diet-induced brain dysfunction in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, HF diet, or HF diet with 0.5% GTEs (HFGT) for four months. The HF diet reduced memory retention and induced amyloid &#946;1&#8211;42 accumulation, whereas GTEs attenuated these changes. In HF diet-fed mice, lipid oxidative stress, assessed by malondialdehyde levels, was increased. The levels of proteins that promote synaptic plasticity, such as brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95), were reduced. These alterations related to brain dysfunction were not observed in HFGT diet-fed mice. Overall, our data suggest that GTEs intake might attenuate brain dysfunction in HF diet-fed SAMP8 mice by protecting synaptic plasticity as well as via anti-oxidative effects. In conclusion, GTEs might ameliorate unhealthy diet-induced brain dysfunction that develops with aging

Phosphorylation of kinases involved in insulin signaling in skeletal muscle of adult (6M) SAMP8 mice.

<p>Representative western blot images (upper panels, all images provided in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0195753#pone.0195753.s001" target="_blank">S1 Appendix</a>) and quantification of phosphorylation (lower graphs) are shown for Akt (A) and S6K (B). Data are means ± S.D. One-way ANOVA followed by Tukey’s post-hoc test was used for comparison among groups. *, <i>P</i> < 0.05.</p