Targeted Telehealth Education Increases Interest in Using Telehealth among a Diverse Group of Low-Income Older Adults.

Telehealth allows older adults to take control over their health and preventive care; however, they are less likely to use telehealth. Minority older adults use telehealth services less than their White counterparts. During COVID-19, the U.S. Medicare system allowed for telehealth delivery of Annual Wellness Visits, which are known to improve use of preventive services. To increase telehealth use, we targeted vulnerable, low-income, minority older adults and provided education to improve knowledge of and identify barriers to telehealth use. Ultimately, this could serve as a means of improving health and preventive care services. Participants resided at independent living facilities, low-income housing, and elders of the Native American coalition; N = 257. Participants received written education materials; a subset attended a 20-min presentation. In this quasi-experimental study, participants completed a pre-post survey. Results were analyzed using Chi-Squared and Fisher's Exact tests. Participants included 54 'in-person' and 203 'at-home' learners. Most were female (79%), single/widowed (51%), and white (65%). At baseline, 39% were familiar with telehealth; following education 73% stated understanding on accessing telehealth. Nearly 40% of participants said they would use telehealth in the future; a larger proportion of "in-person" (73%) learners were willing to use telehealth than "at-home" learners (41%) (p = 0.001). Divorced older adults and Blacks voiced greater likelihoods of using telehealth than their married/widowed and White counterparts, respectively (Χ2(3, N = 195) = 9.693, p = 0.02), (p = 0.01). This education program demonstrates an increase likelihood in health promotion among older adults by increasing confidence in accessing and future use of telehealth; therefore, we achieved our aim of promoting telehealth use and improving health promotion.

A pen pal program during COVID-19 pandemic increases student interest for careers in geriatrics.

Social isolation and loneliness are serious issues facing older adults that have been intensified during COVID-19. Through a pen pal program, we connected 69 healthcare professional students with 180 older adults in our community to help reduce social isolation and loneliness. Participants were connected through letters, e-mails, and phone calls for three months. At the end of the program, we surveyed students (response rate: 62%). Half of the students reported spending less than 20 minutes per week on the project. Of the survey respondents roughly 91% were white, 74.4% were enrolled in the College of Medicine, and 51.1% were in their first year of their respective program. Students increased their knowledge of social isolation and loneliness (p = .0001), their interest in volunteering (p = .018) and working with older adults (p = .028), and their comfort communicating with older adults (p = .002). Students reported that their wellness improved and that they practiced skills that would be used in their future careers. By providing volunteer experiences to students, we can increase their exposure to the geriatric population, hopefully increasing the number of students who enter geriatrics while simultaneously reducing social isolation and loneliness in older adults.

LXRalpha activation perturbs hepatic insulin signaling and stimulates production of apolipoprotein B-containing lipoproteins.

Liver X receptor-alpha (LXRalpha) is considered a master regulator of hepatic lipid metabolism; however, little is known about the link between LXR activation, hepatic insulin signaling, and very low-density lipoprotein (VLDL)-apolipoprotein B (apoB) assembly and secretion. Here, we examined the effect of LXRalpha activation on hepatic insulin signaling and apoB-lipoprotein production. In vivo activation of LXRalpha for 7 days using a synthetic LXR agonist, TO901317, in hamsters led to increased plasma triglyceride (TG; 3.6-fold compared with vehicle-treated controls, P = 0.006), apoB (54%, P < 0.0001), and VLDL-TG (eightfold increase compared with vehicle). As expected, LXR stimulation activated maturation of sterol response element binding protein-1c (SREBP-1c) as well as the SREBP-1c target genes steroyl CoA desaturase (SCD) and fatty acid synthase (FAS). Metabolic pulse-chase labeling experiments in primary hamster hepatocytes showed increased stability and secretion of newly synthesized apoB following LXR activation. Microsomal triglyceride transfer protein (MTP) mRNA and protein were unchanged, however, likely because of the relatively short period of treatment and long half-life of MTP mRNA. Examination of hepatic insulin-signaling molecules revealed LXR-mediated reductions in insulin receptor (IR)beta subunit mass (39%, P = 0.014) and insulin receptor substrate (IRS)-1 tyrosine phosphorylation (24%, P = 0.023), as well as increases in protein tyrosine phosphatase (PTP)1B (29%, P < 0.001) protein mass. In contrast to IRS-1, a twofold increase in IRS-2 mass (228%, P = 0.0037) and a threefold increase in IRS-2 tyrosine phosphorylation (321%, P = 0.012) were observed. In conclusion, LXR activation dysregulates hepatic insulin signaling and leads to a considerable increase in the number of circulating TG-rich VLDL-apoB particles, likely due to enhanced hepatic assembly and secretion of apoB-containing lipoproteins.

Metabolic effects of dietary cholesterol in an animal model of insulin resistance and hepatic steatosis.

Although the atherogenic role of dietary cholesterol has been well established, its diabetogenic potential and associated metabolic disturbances have not been reported. Diet-induced hamster models of insulin resistance and dyslipidemia were employed to determine lipogenic and diabetogenic effects of dietary cholesterol. Metabolic studies were conducted in hamsters fed diets rich in fructose (40%), fat (30%), and cholesterol (0.05-0.25%) (FFC) and other test diets. Short-term feeding of the FFC diet induced insulin resistance, glucose intolerance, hypertriglyceridemia, and hypercholesterolemia. Prolonged feeding (6-22 wk) of the FFC diet led to severe hepatic steatosis, glucose intolerance, and mild increases in fasting blood glucose, suggesting progression toward type 2 diabetes, but did not induce beta-cell dysfunction. Metabolic changes induced by the diet, including dyslipidemia and insulin resistance, were cholesterol concentration dependent and were only markedly induced on a high-fructose and high-fat dietary background. There were significant increases in hepatic and plasma triglyceride with FFC feeding, likely due to a 10- to 15-fold induction of hepatic stearoyl-CoA desaturase compared with chow levels (P < 0.03). Hepatic insulin resistance was evident based on reduced tyrosine phosphorylation of the insulin receptor-beta, IRS-1, and IRS-2 as well as increased protein mass of protein tyrosine phosphatase 1B. Interestingly, nuclear liver X receptor (LXR) target genes such as ABCA1 were upregulated on the FFC diet, and dietary supplementation with an LXR agonist (instead of dietary cholesterol) worsened dyslipidemia, glucose intolerance, and upregulation of target mRNA and proteins similar to that of dietary cholesterol. In summary, these data clearly implicate dietary cholesterol, synergistically acting with dietary fat and fructose, as a major determinant of the severity of metabolic disturbances in the hamster model. Dietary cholesterol appears to induce hepatic cholesterol ester and triglyceride accumulation, and diet-induced LXR activation (via cholesterol-derived oxysterols) may possibly be one key underlying mechanism.

Dietary fructose and the metabolic syndrome.

PURPOSE OF REVIEW: Fructose, a naturally found sugar in many fruits, is now commonly used as an industrial sweetener and is excessively consumed in Western diets. High fructose intake is increasingly recognized as causative in development of prediabetes and metabolic syndrome. The mechanisms underlying fructose-induced metabolic disturbances are unclear but are beginning to be unravelled. This review presents recent findings in this field and an overall mechanistic insight into the metabolic effects of dietary fructose and its role in metabolic syndrome. RECENT FINDINGS: Recent animal studies have confirmed the link between fructose feeding and increased plasma uric acid, a potentially causative factor in metabolic syndrome. Advanced glycation end products are also implicated because of their direct protein modifications and indirect effects on inflammation and oxidative stress. Human studies have demonstrated fructose's ability to change metabolic hormonal response, possibly contributing to decreased satiety. SUMMARY: There is much evidence from both animal models and human studies supporting the notion that fructose is a highly lipogenic nutrient that, when consumed in high quantities, contributes to tissue insulin insensitivity, metabolic defects, and the development of a prediabetic state. Recently evidence has helped to decipher the mechanisms involved in these metabolic changes.

Lipopolysaccharide accelerates caspase-independent but cathepsin B-dependent death of human lung epithelial cells.

Caspase-independent cell death has drawn increasing attention. In the present study, we found that lipopolysaccharide (LPS) accelerated spontaneous death of human lung epithelial A549 cells in a serum- and cell density-dependent manner: while serum starvation has been demonstrated to induce apoptosis in the same cell line, LPS-induced cell death was only observed in the presence of serum; in addition, the cell death was not observed when the cells were seeded at 10- or 100-fold lower density. The apoptotic features were demonstrated by TUNEL assay, DNA laddering and Annexin V staining. However, treatment of cells with two commonly used pan-caspase inhibitors, zVAD.fmk or BOC-D.fmk, failed to block cell death. In contrast, two cathepsin B inhibitors, Ca074-Me or N-1845, reduced cell death significantly. A time-dependent activation of cathepsin B, but not caspase 3, was observed in both control and LPS-treated cells. Although LPS did not further activate cathepsin B or its release, it increased expression and translocation of apoptosis inducing factor from mitochondria to the nucleus, and increased release of cytochrome c from mitochondria. LPS-induced cell death was significantly attenuated by either N-acetyl-L-cysteine or pyrrolidine-dithiocarbamate, both free radical scavengers. Disruption of lipid raft formation with filipin or methyl-beta-cyclodextrin also reduced apoptosis significantly, suggesting that lipid raft-dependent signaling is essential. These data imply that confluent cells undergo spontaneous cell death mediated by cathepsin B; LPS may accelerate this caspase-independent cell death through release of mitochondrial contents and reactive oxygen species.