Stress and excessive alcohol consumption among insured and uninsured adults during the COVID-19 pandemic.

Aim: This study examined the relationships between stress, excessive drinking, including binge and heavy drinking, and health insurance status among a regionally representative sample of adults living in Northern Larimer County, Colorado, during the COVID-19 pandemic. Subject and methods: Data from 551 adults aged 18 to 64 years (62.98% aged 45 to 65 years; 73.22% female; 92.98% non-Hispanic White) were used. The sample was weighted by age and binary sex. A series of logistic regressions were applied to examine bivariate associations among stress, drinking, and health insurance status, with and without accounting for the effects of sociodemographic and health-related covariates. Stratified analyses were applied to explore differential associations of stress and drinking among individuals with different health insurance coverage. Results: A total of 23.23% of the adult sample reported binge drinking, and 16.15% reported heavy drinking; 10.53% of the sample reported both binge and heavy drinking. Individuals with higher levels of stress were more likely to report binge drinking (OR: 1.65; 95% CI: 1.65, 1.68) and heavy drinking (OR: 2.61; 95% CI: 2.54, 2.67), after adjusting for sociodemographic and health-related covariates. Relative to individuals with private health insurance coverage, adults enrolled in Medicaid and those without health insurance coverage were more susceptible to the effect of stress on binge and heavy drinking. Conclusion: Our results highlighted a need for continuing statewide and/or national efforts in closing the insurance coverage gap and providing affordable marketplace health insurance in the hope of preventing excessive drinking due to high levels of stress during a challenging time.

Combination of deep sea water and Sesamum indicum leaf extract prevents high-fat diet-induced obesity through AMPK activation in visceral adipose tissue.

The aim of the present study was to evaluate the protective effects of a combination of deep sea water (DSW) and Sesamum indicum leaf extract (SIE) against high-fat diet (HFD)-induced obesity and investigate its molecular mechanisms in adipose tissue. ICR mice were randomly divided into three groups: HFD control (HFC), DSW and DSW + 125 mg/kg SIE (DSS) groups. The mice in the HFC group had free access to drinking water while those in the DSW and DSS groups had free access to DSW. The mice in the DSS group were treated with SIE once per day for 8 weeks. The mice in all three groups were allowed to freely access a HFD. Compared with the HFC group, the DSS group showed lower body weight gain and serum levels of glucose, triglycerides and leptin. Histological analyses of the epididymal white, retroperitoneal white and scapular brown adipose tissue of mice in the DSS group revealed that the adipocytes were markedly decreased in size compared with those in the HFC group. Moreover, DSS significantly increased the levels of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase (ACC) in mice epididymal adipose tissues. Furthermore, DSS upregulated the expression levels of lipolysis-associated mRNA, specifically peroxisome proliferator-activated receptor-α (PPAR-α) and cluster of differentiation 36 (CD36), and energy expenditure-associated mRNA, namely uncoupling protein 2 (UCP2) and carnitine palmitoyltransferase-1 (CPT1) in the epididymal adipose tissues. By contrast, DSS suppressed the expression of the lipogenesis-related gene sterol regulatory element-binding protein-1 (SREBP1) at the mRNA level. These results suggest that DSS is effective for suppressing body weight gain and enhancing the lipid profile.

Bee venom protects SH-SY5Y human neuroblastoma cells from 1-methyl-4-phenylpyridinium-induced apoptotic cell death.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by progressive selective loss of dopaminergic neurons in the substantia nigra. Recently, bee venom was reported to protect dopaminergic neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induced mice PD model, however, the underlying mechanism is not fully understood. The objective of the present study is to investigate the neuroprotective mechanism of bee venom against Parkinsonian toxin, 1-methyl-4-phenylpyridine (MPP(+)), in SH-SY5Y human neuroblastoma cells. Our results revealed that bee venom pretreatment (1-100 ng/ml) increased the cell viability and decreased apoptosis assessed by DNA fragmentation and caspase-3 activity assays in MPP(+)-induced cytotoxicity in SH-SY5Y cells. Bee venom increased the anti-apoptotic Bcl-2 expression and decreased the pro-apoptotic Bax, cleaved PARP expressions. In addition, bee venom prevented the MPP(+)-induced suppression of Akt phosphorylation, and the neuroprotective effect of bee venom against MPP(+)-induced cytotoxicity was inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002. These results suggest that the anti-apoptotic effect of bee venom is mediated by the cell survival signaling, the PI3K/Akt pathway. These results provide new evidence for elucidating the mechanism of neuroprotection of bee venom against PD.

Beneficial effects of IH-901 on glucose and lipid metabolisms via activating adenosine monophosphate-activated protein kinase and phosphatidylinositol-3 kinase pathways.

IH-901 is an intestinal metabolite of ginsenosides found in Panax ginseng. In the present study, effects of IH-901 on glucose and lipid metabolisms were examined using C2C12 myotubes and C57BL/ksJ db/db mice. A significant increase in phosphorylated adenosine monophosphate-activated protein kinase was observed when differentiated C2C12 myotubes were treated with IH-901. Glucose transporter 4 protein expressions were also up-regulated when muscle cells were treated with of IH-901 up to 60 minutes, resulting in stimulation of glucose uptake by 25% as compared with untreated cells. In addition, phosphatidylinositol-3 kinase and Akt protein expressions were increased when C2C12 myotubes were exposed to IH-901 for up to 3 hours; and these effects including glucose uptake were attenuated by pretreatment with LY294002, a selective phosphatidylinositol-3 kinase inhibitor. In animal study, IH-901 at 25 mg/kg lowered the plasma glucose, triglyceride, cholesterol, and nonesterified fatty acid levels by 20.7%, 41.6%, 20.2%, and 24.6%, respectively, compared with control mice. In the meantime, plasma insulin levels were significantly increased by 2.2 and 3.4 times in 10 and 25 mg/kg-treated mice, respectively, compared with control mice, in parallel with the histologic observation showing a preserved architecture of the pancreatic islet. Protein and gene expression patterns for adenosine monophosphate-activated protein kinase, sterol regulatory element binding protein-1a, and glucose transporter 4 in the liver and skeletal muscles were similar to those in cell studies. In summary, IH-901 might be a promising therapeutic agent improving altered glucose and lipid metabolisms revealed in type 2 diabetes mellitus patients.

An active part of Artemisia sacrorum Ledeb. attenuates hepatic lipid accumulation through activating AMP-activated protein kinase in human HepG2 cells.

Artemisia sacrorum Ledeb. (Compositae) (ASL) is a traditional Chinese medicine used to treat different hepatic diseases. However, a hypolipidemic effect of ASL on fatty liver disease has not been reported. Therefore, we investigated whether 95% ethanol eluate (EE), an active part of ASL, would attenuate hepatic lipid accumulation in human HepG2 cells by activating AMP-activated protein kinase (AMPK). Significant decreases in triglyceride levels and increases in AMPK and acetyl-CoA carboxylase (ACC) phosphorylation were observed when the cells were treated with 95% EE. EE down-regulated the lipogenesis gene expression of sterol regulatory element-binding protein 1c (SREBP1c) and its target genes, such as fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD1), in a time- and dose-dependent manner. In contrast, the lipolytic gene expression of peroxisome proliferator-activated receptor alpha (PPAR-alpha) and CD36 increased in a time- and dose-dependent manner. These effects were abolished by pretreatment with compound C, an AMPK inhibitor. However, there were no differences in the gene expression of SREBP2, low density lipoprotein receptor (LDLR), hydroxymethyl glutaryl CoA reductase (HMG-CoA), or glucose transporter 2 (GLUT2). At the same time, 95% EE significantly increased the gene expression of acyl CoA oxidase (ACOX) in a time- and dose-dependent manner. Thus, AMPK mediated 95% EE induced suppression of SREBP1c and activation of PPAR-alpha respectively. These finding indicate that 95% EE attenuates hepatic lipid accumulation through AMPK activation and may be active in the prevention of serious diseases such as fatty liver, obesity, and type-2 diabetic mellitus.

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway.

20(S)-ginsenoside Rg3 [20(S)-Rg3)], one of the main constituents isolated from Panax ginseng, has been shown to have an anti-cancer effect and to induce apoptosis by interfering with several signaling pathways. However, the molecular mechanisms of AMP-activated protein kinase (AMPK) associated with apoptosis in HT-29 colon cancer cells remain unclear. In the present study, we investigated whether 20(S)-Rg3 exerts an anti-proliferative effect and induces apoptosis by modulating the AMPK signaling pathway in HT-29 cells. 20(S)-Rg3-treated cells displayed several apoptotic features, including DNA fragmentation, proteolytic cleavage of poly (ADP-ribose) polymerase (PARP) and morphological changes. 20(S)-Rg3 down-regulated the expression of anti-apoptotic protein B-cell CLL/lymphoma 2 (Bcl2), up-regulated the expression of pro-apoptotic protein of p53 and Bcl-2-associated X protein (Bax), and caused the release of mitochondrial cytochrome c, PARP, caspase-9 and caspase-3. However, 20(S)-Rg3-induced apoptosis was completely abolished in the presence of compound C (AMPK inhibitor) or small interfering RNA for AMPK (siAMPK). In addition, STO-609 (CaMKKß inhibitor) attenuated 20(S)-Rg3-induced AMPK activation and apoptosis. These results suggest that 20(S)-Rg3-induced apoptosis in HT-29 cells is mediated via the AMPK signaling pathway, and that 20(S)-Rg3 is capable of inducing apoptosis in colon cancer.

Protective effects of fermented ginseng on streptozotocin-induced pancreatic beta-cell damage through inhibition of NF-kappaB.

Ginseng (Panax ginseng C.A. Meyer) is widely used in Asian countries as a traditional medicine for the treatment of various diseases. It is known to have anti-inflammatory effects, although the mechanism is not clear. In this study, preventive effects of fermented ginseng (FG) against streptozotocin (STZ)-induced pancreatic beta-cell death was assessed in RINm5F insulinoma cells. FG markedly inhibited the production of nitrite in a dose-dependent manner. The decrease in nitrite production was found to correlate with reduced inducible nitric oxide (iNOS) protein and mRNA levels. To characterize the anti-inflammatory mechanism of FG at the transcriptional level, we examined effects of FG on the activity of nuclear factor-kappaB (NF-kappaB). FG reduced a translocation of the NF-kappaB subunit and NF-kappaB-dependent transcriptional activity. FG blocked signaling upstream of NF-kappaB activation, such as degradation of inhibitor factor-kappaBalpha (IkappaBalpha ) and phosphorylations of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK). These results suggest that FG protects against STZ-induced pancreatic beta-cell damage by downregulation of iNOS, cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-alpha ) gene expressions by blocking NF-kappaB and mitogen-activated protein kinase activities.