Nutrition and Healthy Aging最新文献

{"title":"A central role for hypoxia-inducible factor (HIF)-2α in hepatic glucose homeostasis.","authors":"Sadeesh K Ramakrishnan,&nbsp;Yatrik M Shah","doi":"10.3233/NHA-170022","DOIUrl":"https://doi.org/10.3233/NHA-170022","url":null,"abstract":"<p><p>Hepatic glucose production is regulated by hormonal and dietary factors. At fasting, 80% of glucose released into the circulation is derived from the liver, among which gluconeogenesis accounts for 55% and the rest by glycogenolysis. Studies suggest a complex mechanism involved in the regulation of hepatic glucose metabolism during fasting and post-absorptive phase. Oxygen plays a key role in numerous metabolic pathways such as TCA cycle, gluconeogenesis, glycolysis and fatty acid oxidation. Oxygenation of the gastrointestinal tract including liver and intestine is dynamically regulated by changes in the blood flow and metabolic activity. Cellular adaptation to low oxygen is mediated by the transcription factors HIF-1α and HIF-2α. HIF-1α regulates glycolytic genes whereas HIF-2α is known to primarily regulate genes involved in cell proliferation and iron metabolism. This review focuses on the role of the oxygen sensing signaling in the regulation of hepatic glucose output with an emphasis on hypoxia inducible factor (HIF)-2α. Recent studies have established a metabolic role of HIF-2α in systemic glucose homeostasis. Understanding the HIF-2α dependent mechanism in hepatic metabolism will greatly enhance our potential to utilize the oxygen sensing mechanisms to treat metabolic diseases.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 3","pages":"207-216"},"PeriodicalIF":0.0,"publicationDate":"2017-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-170022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35687125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ras signaling in aging and metabolic regulation.","authors":"Cathy Slack","doi":"10.3233/NHA-160021","DOIUrl":"10.3233/NHA-160021","url":null,"abstract":"<p><p>Aberrant signal transduction downstream of the Ras GTPase has a well-established role in tumorigenesis. Mutations that result in hyperactivation of Ras are responsible for a third of all human cancers. Hence, small molecule inhibitors of the Ras signal transduction cascade have been under intense focus as potential cancer treatments. In both invertebrate and mammalian models, emerging evidence has also implicated components of the Ras signaling pathway in aging and metabolic regulation. Here, I review the current evidence for Ras signaling in these newly discovered roles highlighting the interactions between the Ras pathway and other longevity assurance mechanisms. Defining the role of Ras signaling in maintaining age-related health may have important implications for the development of interventions that could not only increase lifespan but also delay the onset and/or progression of age-related functional decline.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 3","pages":"195-205"},"PeriodicalIF":0.0,"publicationDate":"2017-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ae/24/nha-4-nha160021.PMC5734121.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35687124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydration health literacy in the elderly.","authors":"Dominic Picetti, Stephen Foster, Amanda K Pangle, Amy Schrader, Masil George, Jeanne Y Wei, Gohar Azhar","doi":"10.3233/NHA-170026","DOIUrl":"10.3233/NHA-170026","url":null,"abstract":"<p><strong>Background: </strong>Inadequate hydration in the elderly is associated with increased morbidity and mortality. However, few studies have addressed the knowledge of elderly individuals regarding hydration in health and disease. Gaps in health literacy have been identified as a critical component in health maintenance, and promoting health literacy should improve outcomes related to hydration associated illnesses in the elderly.</p><p><strong>Methods: </strong>We administered an anonymous survey to community-dwelling elderly (<i>n</i> = 170) to gauge their hydration knowledge.</p><p><strong>Results: </strong>About 56% of respondents reported consuming >6 glasses of fluid/day, whereas 9% reported drinking ≤3 glasses. About 60% of respondents overestimated the amount of fluid loss at which moderately severe dehydration symptoms occur, and 60% did not know fever can cause dehydration. Roughly 1/3 were not aware that fluid overload occurs in heart failure (35%) or kidney failure (32%). A majority of respondents were not aware that improper hydration or changes in hydration status can result in confusion, seizures, or death.</p><p><strong>Conclusions: </strong>Overall, our study demonstrated that there were significant deficiencies in hydration health literacy among elderly. Appropriate education and attention to hydration may improve quality of life, reduce hospitalizations and the economic burden related to hydration-associated morbidity and mortality.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 3","pages":"227-237"},"PeriodicalIF":0.0,"publicationDate":"2017-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2d/03/nha-4-nha170026.PMC5734130.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35687127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ceramide dependent lipotoxicity in metabolic diseases","authors":"L. Ying, Trevor S. Tippetts, Bhagirath Chaurasia","doi":"10.3233/NHA-170032","DOIUrl":"https://doi.org/10.3233/NHA-170032","url":null,"abstract":"Sphingolipids, a major class of lipids in cell membranes, play diverse roles in biology. They are synthesized by a highly conserved biosynthetic pathway that leads to the production of ceramides, the major precursors of most complex sphingolipids. Almost all known stress stimuli including inflammatory agonists, chemotherapeutics, and saturated fatty acids induce the synthesis of ceramide and its metabolites. A panoply of recent studies has implicated ceramides in the development of the metabolic comorbidities of obesity such as diabetes and cardiovascular diseases. In particular, inhibition of ceramide biosynthesis in rodents ameliorates insulin resistance, diabetes, cardiomyopathy, atherosclerosis, and steatohepatitis. These data implicate ceramides as major contributors to the development of metabolic diseases. This review summarizes recent findings on this emerging class of bioactive lipids with an emphasis on studies using in vivo models to understand their role in metabolic disease.","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-170032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44025529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian clocks, diets and aging.","authors":"Amol Chaudhari,&nbsp;Richa Gupta,&nbsp;Kuldeep Makwana,&nbsp;Roman Kondratov","doi":"10.3233/NHA-160006","DOIUrl":"https://doi.org/10.3233/NHA-160006","url":null,"abstract":"<p><p>Diets and feeding regimens affect many physiological systems in the organism and may contribute to the development or prevention of various pathologies including cardiovascular diseases or metabolic syndromes. Some of the dietary paradigms, such as calorie restriction, have many well-documented positive metabolic effects as well as the potential to extend longevity in different organisms. Recently, the circadian clocks were put forward as integral components of the calorie restriction mechanisms. The circadian clocks generate the circadian rhythms in behavior, physiology, and metabolism; circadian disruption is associated with reduced fitness and decreased longevity. Here we focus on recent advances in the interplay between the circadian clocks and dietary paradigms. We discuss how the regulation of the circadian clocks by feeding/nutrients and regulation of nutrient signaling pathways by the clocks may contribute to the beneficial effects of calorie restriction on metabolism and longevity, and whether the circadian system can be engaged for future medical applications.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 2","pages":"101-112"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-160006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34945891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary polyunsaturated fatty acids and their metabolites: Implications for diabetes pathophysiology, prevention, and treatment.","authors":"Joshua C Neuman, Rachel J Fenske, Michelle E Kimple","doi":"10.3233/NHA-160004","DOIUrl":"10.3233/NHA-160004","url":null,"abstract":"","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 2","pages":"127-140"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/55/39/nha-4-nha160004.PMC5391679.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34945894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A randomized trial of the effects of the no-carrageenan diet on ulcerative colitis disease activity.","authors":"Sumit Bhattacharyya,&nbsp;Theresa Shumard,&nbsp;Hui Xie,&nbsp;Amar Dodda,&nbsp;Krista A Varady,&nbsp;Leo Feferman,&nbsp;Allan G Halline,&nbsp;Jay L Goldstein,&nbsp;Stephen B Hanauer,&nbsp;Joanne K Tobacman","doi":"10.3233/NHA-170023","DOIUrl":"https://doi.org/10.3233/NHA-170023","url":null,"abstract":"<p><p><b>BACKGROUND:</b> Carrageenan is a very common food additive in Western diets, but predictably causes inflammation in thousands of cell-based and animal experiments. <b>OBJECTIVE:</b> To assess the impact of carrageenan exposure on the interval to relapse in patients with ulcerative colitis in remission. <b>METHODS:</b> A randomized, double-blind, placebo-controlled, multicenter, clinical trial was conducted to assess if patients with ulcerative colitis in remission would have a longer interval to relapse if they followed a diet with no carrageenan. All participants were instructed in the no-carrageenan diet and were randomized to either placebo capsules or carrageenan-containing capsules. The carrageenan in the capsules was less than the average daily carrageenan intake from the diet. Relapse was defined as an increase of two or more points on the Simple Clinical Colitis Activity Index (SCCAI) and intensification of treatment for ulcerative colitis. Participants were followed by telephone calls every two weeks until relapse or one year of participation. The occurrence of relapse and inflammatory biomarkers were compared between the two groups. <b>RESULTS:</b> Twelve patients completed study questionnaires. Three patients who received carrageenan-containing capsules relapsed, and none of the patients who received placebo-containing capsules relapsed (<i>p</i> = 0.046, log-rank test). Laboratory tests showed increases in Interleukin-6 (<i>p</i> = 0.02, paired <i>t</i>-test, two-tailed) and fecal calprotectin (<i>p</i> = 0.06; paired <i>t</i>-test, two-tailed) between the beginning and the end of study participation in the carrageenan-exposed group, but not in the placebo-group. <b>CONCLUSION:</b> Carrageenan intake contributed to earlier relapse in patients with ulcerative colitis in remission. Restriction of dietary carrageenan may benefit patients with ulcerative colitis.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 2","pages":"181-192"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-170023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34946346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA 21 is up-regulated in adipose tissue of obese diabetic subjects.","authors":"Valeria Guglielmi,&nbsp;Monica D'Adamo,&nbsp;Rossella Menghini,&nbsp;Marina Cardellini,&nbsp;Paolo Gentileschi,&nbsp;Massimo Federici,&nbsp;Paolo Sbraccia","doi":"10.3233/NHA-160020","DOIUrl":"https://doi.org/10.3233/NHA-160020","url":null,"abstract":"<p><p>We investigated miR21 expression in omental (OAT) and subcutaneous adipose tissue (SAT) from 16 obese subjects undergoing bariatric surgery. Patients were divided into two age- and BMI-matched groups according to the presence of type 2 diabetes (T2D). miR21 was not differently expressed in OAT and SAT. However, miR21 expression was two folds greater in adipose tissue in patients with T2D. Accordingly, in primary cultures of adipocytes from non diabetic overweight subjects, miR21 expression increased after 24-h exposure to high glucose and insulin. In conclusion, miR21 appears linked to insulin-resistance deterioration within its pathophysiologic progression from obesity to T2D.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 2","pages":"141-145"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-160020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34945893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term calorie restriction in humans is not associated with indices of delayed immunologic aging: A descriptive study.","authors":"A Janet Tomiyama, Jeffrey M Milush, Jue Lin, James M Flynn, Pankaj Kapahi, Eric Verdin, Elizabeth Sinclair, Simon Melov, Elissa S Epel","doi":"10.3233/NHA-160017","DOIUrl":"10.3233/NHA-160017","url":null,"abstract":"<p><p><b>BACKGROUND:</b> Delayed immunologic aging is purported to be a major mechanism through which calorie restriction (CR) exerts its anti-aging effects in non-human species. However, in non-obese humans, the effect of CR on the immune system has been understudied relative to its effects on the cardiometabolic system. <b>OBJECTIVE:</b> To examine whether CR is associated with delayed immunologic aging in non-obese humans. <b>METHODS:</b> We tested whether long-term CR practitioners (average 10.03 years of CR) evidenced decreased expression of T cell immunosenescence markers and longer immune cell telomeres compared to gender-, race/ethnicity-, age-, and education-matched \"healthy\" Body Mass Index (BMI) and \"overweight\"/\"obese\" BMI groups. <b>RESULTS:</b> Long-term human CR practitioners had lower BMI (<i>p</i> <  0.001) and fasting glucose (<i>p</i> <  0.001), as expected. They showed similar frequencies of pre-senescent cells (CD8⁺CD28^- T cells and CD57 and PD-1 expressing T cells) to the comparison groups. Even after adjusting for covariates, including cytomegalovirus status, we observed shorter peripheral blood mononuclear cell telomeres in the CR group (<i>p</i> = 0.012) and no difference in granulocyte telomeres between groups (<i>p</i> = 0.42). <b>CONCLUSIONS:</b> We observed no clear evidence that CR as it is currently practiced in humans delays immune aging related to telomere length or T cell immunosenescent markers.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 2","pages":"147-156"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-160017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34946342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of reduced <i>rpd3</i> levels on fly physiology.","authors":"Jared K Woods,&nbsp;Tahereh Ziafazeli,&nbsp;Blanka Rogina","doi":"10.3233/NHA-160016","DOIUrl":"https://doi.org/10.3233/NHA-160016","url":null,"abstract":"<p><p><b>BACKGROUND:</b> Rpd3 is a conserved histone deacetylase that removes acetyl groups from lysine residues within histones and other proteins. Reduction or inhibition of Rpd3 extends longevity in yeast, worms, and flies. Previous studies in flies suggest an overlap with the mechanism of lifespan extension by dietary restriction. However, the mechanism of <i>rpd3</i>'s effects on longevity remains unclear. <b>OBJECTIVES:</b> In this study we investigated how <i>rpd3</i> reduction affects fly spontaneous physical activity, fecundity, and stress resistance. <b>METHODS:</b> We examined the effects of <i>rpd3</i> reduction on fly spontaneous physical activity by using population monitors, we determined female fecundity by counting daily egg laying, and we determined fly survivorship in response to starvation and paraquat. <b>RESULTS:</b> In flies, <i>rpd3</i> reduction increases peak spontaneous physical activity of <i>rpd3 ^<i>def</i></i> male flies at a young age but does not affect total 24 hour activity. Male and female <i>rpd3 ^<i>def</i></i> mutants are more resistant to starvation on low and high calorie diets. In addition, increased resistance to paraquat was observed in females of one allele. A decrease in <i>rpd3</i> levels does not affect female fecundity. <b>CONCLUSIONS:</b> A decrease in <i>rpd3</i> levels mirrors some but not all changes associated with calorie restriction, illustrated by an increased peak of spontaneous activity in <i>rpd3 ^<i>def</i></i> /+ heterozygous male flies but no effect on total spontaneous activity and fecundity.</p>","PeriodicalId":37419,"journal":{"name":"Nutrition and Healthy Aging","volume":"4 2","pages":"169-179"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/NHA-160016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34946344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}