Hyperbaric oxygen (HBO) therapy is a treatment modality useful for diseases. Hypoxia could stimulate the induction of insulin resistance. Therefore, we sought to determine whether hyperbaric oxygen would ameliorate insulin sensitivity by promoting glucose transporter type 4 (GLUT4) expression in muscle and by stimulating UCP1 in brown adipose tissue (BAT) in a streptozocin (STZ)-induced type 2 diabetes mellitus (T2DM) mouse model. Male C57BL/6J mice were treated three times with low-dose of streptozocin (60 mg/kg, i.p.) and were fed with high-fat diets (HFD) to establish the T2DM model. HBO was administered daily as 100% oxygen at 2.0 atmosphere absolute (ATA) for 1 h for a week. We found that HBO significantly reduced blood glucose levels and attenuated insulin resistance in T2DM mice. HBO modulated food intake by influencing the activity of neuropeptide Y (NPY)-positive neurons in the arcuate nucleus (Arc). HBO treatment increased GLUT4 amount and level of phosphorylated Akt (p-Akt) in muscles of T2DM mice whereas this treatment stimulated the phosphorylation of AMPK in muscles of both T2DM and HFD mice. The morphological staining of BAT and the increased expression of uncoupling of protein 1 (UCP1) demonstrated the promotion of metabolism after HBO treatment. These findings suggest that HBO ameliorates insulin sensitivity of T2DM mice by stimulating the Akt signaling pathway and by promoting GLUT4 expression in muscle, and by increasing UCP1 expression in BAT.

Gestational diabetes mellitus (GDM) poses a significant health risk to pregnant women, and thus exploring the potential underlying mechanism is highly desirable. The aim of the study was to compare maternal serum, cord blood serum, and placental angiopoietin-like 8 (ANGPTL8) levels in the third trimester of pregnancy in women with and without gestational diabetes and explore the potential underlying mechanism. A total of 42 pregnant women (23 with GDM and 19 with normal glucose tolerance (NGT)) along with 29 age-matched non-pregnant healthy females were enrolled. All pregnant subjects were in the late third trimester. Maternal serum and cord blood serum ANGPTL8 levels were measured with an enzyme-linked immunosorbent assay and the protein levels of ANGPTL8 in placentas were assessed with western blotting. The associations between maternal serum and cord blood serum ANGPTL8 levels and metabolic parameters were investigated with the Spearman correlation analysis. Significantly lower levels of maternal serum and placental ANGPTL8 levels were observed in GDM patients compared to NGT pregnant women, while remarkably higher ANGPTL8 levels were present in the cord blood serum samples. The maternal serum ANGPTL8 level was positively correlated with BMI, total cholesterol, triglycerides, and AUC for OGTT and birthweight. Additionally, the cord blood serum ANGPTL8 level was positively correlated with insulin and the homeostatic model assessment for insulin resistance. Both maternal serum and cord blood serum ANGPTL8 levels seemed to correlate with GDM and has the potential to be used as a biomarker for GDM and birthweight prediction.

Type 1 diabetes mellitus (T1dM) is an autoimmune disorder for which the only effective therapy is insulin replacement. Hyperbaric oxygen (HBo) therapy has demonstrated potential in improving hyperglycemia and as a treatment option for T1dM. Ghrelin and HBo have been previously reported to exert proliferative, anti-apoptotic and anti-inflammatory effects in pancreatic cells. The present study investigated the mechanism underlying HBo-and ghrelin system-mediated regulation of glucose metabolism. Male c57Bl/6 mice were intraperitoneally injected with streptozotocin (STZ; 150 mg/kg) to induce T1dM before the diabetic mice were randomly assigned into the T1dM and T1dM + HBo groups. Mice in the T1dM + HBo group received HBo (1 h; 100% oxygen; 2 atmospheres absolute) daily for 2 weeks. Significantly lower blood glucose levels and food intake were observed in mice in the T1dM + HBo group. Following HBo treatment, islet β-cell area were increased whereas those of α-cell were decreased in the pancreas. in addition, greater hepatic glycogen storage in liver was observed, which coincided with higher pancreatic glucose transporter 2 (GluT2) expression levels and reduced hepatic GluT2 membrane trafficking. There were also substantially higher total plasma ghrelin concentrations and gastric ghrelin-o-acyl transferase (GoaT) expression levels in mice in the T1dM + HBo group. HBo treatment also abolished reductions in pancreatic GoaT expression levels in T1dM mice. additionally, hepatic growth hormone secretagogue receptor-1a levels were found to be lower in mice in the T1dM + HBo group compared with those in the T1dM group. These results suggest that HBo administration improved glucose metabolism in a STZ-induced T1dM mouse model. The underlying mechanism involves improved insulin-release, glucose-sensing and regulation of hepatic glycogen storage, an observation that was also likely dependent on the ghrelin signalling system.

Background: Radiotherapy is a routine treatment for pelvic cancer patients. While it had been proven effective, gastrointestinal side effects remain a concern, impairing the quality of life. A few studies focused on the effects of hyperbaric oxygen (HBO) treatment to alleviate radiation-induced gastrointestinal complications. This meta-analysis aimed to critically review and summarize existing literature, assessing the effectiveness of HBO therapy for the treatment of radiation-induced gastrointestinal side effects. Methods: Medical literature search was performed with PubMed, Cochrane Library, and EMBASE up to March 14, 2019. Literatures about HBO treatment upon patients undergoing pelvic cancer (endometrial, cervix, rectum, or prostate cancers) radiotherapy were collected, and the effects of HBO treatment on radiotherapy-induced gastrointestinal complications were evaluated. A random-effects model was used to calculate the pooled effect size. Subgroup analyses were performed to search for sources of heterogeneity. Publication bias was detected with Funnel plots and Egger's test. Results: Three different radiotherapy-related gastrointestinal complications, including rectal bleeding, diarrhea, and pain, were analyzed after screening. It was revealed that the improvement rates were considerable in rectal bleeding (0.81, 95% CI: 0.74-0.89) and diarrhea (0.75, 95% CI: 0.61-0.90) and slightly in pain (0.58, 95% CI: 0.38-0.79). Subgroup analysis revealed factors that significantly influenced the heterogeneity of rectal bleeding, diarrhea, and pain (evaluation criteria, follow-up time, and scoring system, respectively). No significant publication bias was detected. Conclusion: HBO treatment might have the potential to alleviate radiotherapy-related gastrointestinal complications, including rectal bleeding, diarrhea, and pain, but more data are needed for further conclusions. Other symptoms were not further analyzed, as the number of studies was insufficient. More large-scale and prospective studies are needed for better evaluation of HBO's therapeutic values.

This paper introduces a methodology for inverse-modeling of yarn-level mechanics of cloth, based on the mechanical response of fabrics in the real world. We compiled a database from physical tests of several different knitted fabrics used in the textile industry. These data span different types of complex knit patterns, yarn compositions, and fabric finishes, and the results demonstrate diverse physical properties like stiffness, nonlinearity, and anisotropy. We then develop a system for approximating these mechanical responses with yarn-level cloth simulation. To do so, we introduce an efficient pipeline for converting between fabric-level data and yarn-level simulation, including a novel swatch-level approximation for speeding up computation, and some small-but-necessary extensions to yarn-level models used in computer graphics. The dataset used for this paper can be found at http://mslab.es/projects/YarnLevelFabrics.

Little is known about the influence of central nesfatin‐1 on lipid metabolism under diabetic conditions. The main objective of this study was to characterize the mechanisms by which central nesfatin‐1 regulates lipid metabolism in streptozotocin (STZ)‐induced type 2 diabetes mellitus (T2DM) and whether the sympathetic nervous system is involved. Male Kunming mice were fed high‐fat diets (HFDs) and were treated twice with low‐dose STZ (100 mg/kg, intraperitoneal [IP]) to generate the T2DM model. Pharmacological adrenergic blockage (phentolamine 10 mg/kg, propranolol 0.017 mmol) and surgical denervation of sympathetic nervous system of the hindlimb and inguinal fat were used to block nerve conduction to determine whether the effect of central nesfatin‐1 required the hypothalamic‐sympathetic nervous system axis. Plasma free fatty acid (FFA) and insulin levels were measured. AMP‐activated protein kinase (AMPK) levels in skeletal muscle and hormone‐sensitive lipase and adipose triglycerides lipase (HSL/ATGL) levels in white adipose tissue (WAT) were measured using western blot. mRNA expression of AMPK was measured. We found that there were significantly fewer NUCB2/nesfatin‐1 immunoreactive neurons in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) in T2DM mice. Central nesfatin‐1 administration decreased levels of plasma FFA significantly and activated AMPK to enhance fatty‐acid oxidation in skeletal muscle in T2DM mice. In addition, HSL and ATGL were significantly activated during triglyceride mobilization in WAT triggered by central nesfatin‐1 administration. Adrenergic blockade and morphological denervation of the sciatic and femoral nerves reduced these changes. Taken together, these data suggest that central nesfatin‐1 regulates peripheral lipid metabolism in type 2 diabetes via the sympathetic nervous system.

Lipid metabolism dysfunction and obesity are serious health issues to human beings. The current study investigated the effects of hyperbaric oxygen (HBO) against high fat diet (HFD)-induced lipid metabolism dysfunction and the roles of L-carnitine. C57/B6 mice were fed with HFD or normal chew diet, with or without HBO treatment. Histopathological methods were used to assess the adipose tissues, serum free fatty acid (FFA) levels were assessed with enzymatic methods, and the endogenous circulation and skeletal muscle L-carnitine levels were assessed with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Additionally, western blotting was used to assess the expression levels of PPARα, CPT1b, pHSL/HSL, and UCP1. HFD treatment increased body/adipose tissue weight, serum FFA levels, circulation L-carnitines and decreased skeletal muscle L-carnitine levels, while HBO treatment alleviated such changes. Moreover, HFD treatment increased fatty acid deposition in adipose tissues and decreased the expression of HSL, while HBO treatment alleviated such changes. Additionally, HFD treatment decreased the expression levels of PPARα and increased those of CPT1b in skeletal muscle, while HBO treatment effectively reverted such changes as well. In brown adipose tissues, HFD increased the expression of UCP1 and the phosphorylation of HSL, which was abolished by HBO treatment as well. In summary, HBO treatment may alleviate HFD-induced fatty acid metabolism dysfunction in C57/B6 mice, which seems to be associated with circulation and skeletal muscle L-carnitine levels and PPARα expression.

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