Journal of the American Aging Association最新文献

{"title":"Effects of dietary restriction on insulin resistance in obese mice.","authors":"R J Feuers, V G Desai, F X Chen, J D Hunter, P H Duffy, E T Oriaku","doi":"10.1007/s11357-000-0010-0","DOIUrl":"10.1007/s11357-000-0010-0","url":null,"abstract":"<p><p>In many cases, development of insulin resistance has been linked to obesity and may contribute to mechanism of aging. The role of diet, irrespective of degree of obesity, in modulating insulin resistance and development of age degeneration disease remains uncertain. Lowered blood glucose levels are commonly associated with diet restriction (DR), which is an intervention shown to successfully retard aging and age associated disease. The effects of DR on blood glucose and insulin resistance were measured in yellow obese (A(vy)/A), lean black (a/a) mice and in another common inbred strain (B6C3F1) (at three different ages). The yellow obese mice become diabetic as a result of an insulin receptor defect which is not clearly understood. Insulin responses and radioinsulin binding were assayed in yellow obese and lean black mice fed either ad libitum (AL) or DR diets (YAL, BAL, YDR and YAL, respectively) at four different circadian intervals. The B6C3F1 controls were fed either AL (CAL) or DR (CDR) and measures were made at six circadian stages and three different ages. Within 23 days, DR produced a significant loss in body weight and a time-dependent 22-55% reduction in basal blood glucose levels in the yellow obese mice. Additionally, exogenous insulin produced circadian stage dependent (at the time of food intake) reductions in blood glucose in the YDR animals that were not present in YAL animals. (125)I-Insulin binding in liver was increased nearly 2-fold in YDR and BDR mice during the time of day that animals were active and eating. (125)I-Insulin binding was two-fold-higher in CDR mice at 4, 12 and >24 months of age. Binding decreased as a function of age in both the CAL and CDR animals. However, even in the >24 month group the CDR animals were found to have levels of binding that were as high as those found in younger CAL liver. The mechanism of action appears to be through resolution of insulin resistance by modulating an insulin receptor defect.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"23 2","pages":"95-101"},"PeriodicalIF":0.0,"publicationDate":"2000-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3455787/pdf/11357_2000_Article_10.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31373511","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":"Antioxidant supplements: Effects on disease and aging in the United States population.","authors":"D Harman","doi":"10.1007/s11357-000-0004-y","DOIUrl":"10.1007/s11357-000-0004-y","url":null,"abstract":"<p><p>Ingestion of antioxidant supplements by the United States (US) population has increased steadily since the mid-1950's. This review tried to determine if the supplements have contributed significantly to beneficial changes in the US during this period. Experimental animal studies have demonstrated that anti-oxidant supplements lower the incidence of a wide variety of diseases and increase life span. Anti-oxidants are associated with similar changes in man. Changes since the mid-1950's in the US population include: 1) ingestion of antioxidant supplements has increased from one percent, or less, to 40-50 percent today. Cost: now 4-5 billion dollars per year, 2) disproportionate increases in the percentage of older individuals as average life expectancy at birth (ALE-B) rose, 3) declining chronic disability in the elderly since 1982, 4) declining cancer mortality since 1991, and 5) the decline in the rate of reported cardiovascular disease beginning in the 1950's which significantly increased further in 1965. The last four changes suggest that the rate of increase in physiological age with time has been slowed. This can be attributed to decreases in the rate of accumulation of free radical-induced aging changes by the joint action of antioxidant supplements/dietary measures, and improvements in conventional measures (CM) which increase ALE-B, e.g., better medical care, nutrition, housing, accident prevention. The contribution by antioxidants to decreases in physiological age is seemingly small compared to that of CM. However, it will grow relative to CM as the amount and duration of supplement use increases and improvements in CM raise ALE-B closer to 85 years, the age associated with optimal living conditions.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"23 1","pages":"25-31"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3455359/pdf/11357_2000_Article_4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31466763","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":"Metabolic mechanisms of longevity: Caloric restriction in mammals and longevity mutations in Caenorhabditis elegans; a common pathway??","authors":"M A Lane","doi":"10.1007/s11357-000-0001-1","DOIUrl":"10.1007/s11357-000-0001-1","url":null,"abstract":"<p><p>Several recent studies in Caenorhabditis elegans have reported significant extension of the lifespan by probable loss of function mutations in various genes. When sequenced, many of these genes exhibited significant homology to genes in the mammalian insulin signaling cascade. For example, the daf-2 gene that has been shown to regulate lifespan in C elegans shares significant sequence homology with the insulin and IGF-1 receptor genes in mammals. Another longevity gene in the nematode, age-1, is homologous with the p110 subunit of phosphatidylinositol 3-kinase in mammals. This enzyme functions early in the mammalian insulin response cascade to influence many important cellular growth and metabolic processes. These findings and others have led to the suggestion that lifespan regulation in nematodes is controlled by a mechanism similar to that involved in lifespan extension by caloric restriction in mammals. Many intriguing similarities exist between these two model systems providing some support for this idea. However, at present there is insufficient data to conclude that similar genes or mechanisms regulate lifespan determination in nematodes and in mammals.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"23 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3455360/pdf/11357_2000_Article_1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31466271","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":"Age-dependent accumulation of advanced glycation endproducts is accelerated in combined hyperlipidemia and hyperglycemia, a process attenuated by L-arginine.","authors":"A Georgescu,&nbsp;D Popov","doi":"10.1007/s11357-000-0005-x","DOIUrl":"https://doi.org/10.1007/s11357-000-0005-x","url":null,"abstract":"<p><p>In this study we have investigated the occurrence of \"classical\" Amadori rearrangement products of AGE-proteins in the vascular mesenteric bed and in the lens of Golden Syrian hamsters (12 weeks old) rendered simultaneous hyperlipidemics-diabetics (HD), or hyperlipidemics (H) for 24 weeks. For the next 4 weeks the hamsters in HD and H groups received by gavage a solution of 3 mM L-arginine, with the intent to look for the potential effects of L-arginine on the fluorescence of tissular AGE-proteins. Age-matched normal hamsters were used as controls (C). The AGE-products of proteins, and the AGE-collagen isolated from the mesenteric bed were quantitated by fluorescence spectroscopy at ex: 370 nm/em: 440 nm. The results showed that: (i) compared to the fluorescence levels of AGE-proteins detected at C goup, in HD group the fluorescence of AGE-proteins was found 2.78 and 7.41 fold increased in the vascular mesenteric bed and lens, respectively; (ii) in H group the fluorescence of AGE-proteins was 2.36 fold augumented in the vascular mesenteric bed, and 5.43 fold in the lens (versus the C goup); (iii) the aging occurring during the 24 weeks of the experiment induced a small increase in AGE-proteins fluorescence in both mesentery (1.76 fold) and lens (3.83 fold), compared to the levels measured in C group at the inception of the study (12 weeks old hamsters); (iv) the fluorescence of AGE-proteins in the vascular mesenteric bed and in the lens of hamsters in HD and H groups correlated with the increase in circulating plasma glucose and cholesterol concentrations throughout the experiment; (v) L-arginine dietary supplementation in HD and H groups, diminished the AGE-collagen fluorescence in the mesentery to ∼ 35% and ∼ 17%, respectively; in the lens the fluorescence of AGE-proteins was reduced to 65-70% of the levels found in HD and H groups (at 24 weeks). This study showed for the first time that simultaneous hyperlipidemia-hyperglycemia induced an enhanced accumulation of fluorescent AGE-proteins in the mesentery and lens (comparatively to the effect of hyperlipidemia and of chronological aging monitored during the experiment), and that in vivo L-arginine administration decreased the fluorescence of tissular AGE-proteins (AGE-collagen included). The latter observation may bring another area of potential intervention in the adjunct efforts to find out inhibitors of AGE formation, and thus to reduce the increased levels of AGE-proteins accumulated in tissues when diabetes is additionally complicated with atherosclerosis.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"23 1","pages":"33-40"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-000-0005-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31466764","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":"Morphologic assessment of oxidative damage: A review.","authors":"T D Oberley,&nbsp;T A Zainal","doi":"10.1007/s11357-000-0003-z","DOIUrl":"https://doi.org/10.1007/s11357-000-0003-z","url":null,"abstract":"<p><p>Biochemical studies have indicated changes in anti-oxidant enzyme activities and increased oxidative damage products in many disease states, particularly aging and diseases associated with aging, such as neurodegenerative diseases and cancer. To try to determine cellular and subcellular localization of oxidative damage, our laboratory has developed quantitative light and electron microscopy immunogold techniques using specific antibodies to oxidative damage products. Results from studies of different pathologic processes are presented, illustrating that both localization and quantitation of oxidative damage products is possible. These analyses give important insights into the nature of various pathologic processes.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"23 1","pages":"17-24"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-000-0003-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31466273","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":"29th annual meeting of the American Aging Association, 14th annual meeting of the American College of Clinical Gerontology, 13th annual grantee conference of the American Federation for Aging Research","authors":"T. Johnson, James Cypse, Sam Henderson, Stuart K. Kim, Chris K Link, J. Lund","doi":"10.1007/s11357-000-0018-5","DOIUrl":"https://doi.org/10.1007/s11357-000-0018-5","url":null,"abstract":"","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"18 1","pages":"163-190"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-000-0018-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52978446","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":"Studies of aging in ames dwarf mice: Effects of caloric restriction.","authors":"J A Mattison,&nbsp;C Wright,&nbsp;R T Bronson,&nbsp;G S Roth,&nbsp;D K Ingram,&nbsp;A Bartke","doi":"10.1007/s11357-000-0002-0","DOIUrl":"https://doi.org/10.1007/s11357-000-0002-0","url":null,"abstract":"<p><p>Ames dwarf mice, which are small and deficient in growth homone (GH), prolactin (PRL), and thyroid stimulating hormone (TSH) live much longer (1-1.25 years) than their normal siblings. It was of interest to examine the response of these animals to caloric restriction (CR) because of the possibility that dwarf mice are voluntarily caloric restricted. We are testing the hypothesis that this possible natural caloric restriction will negate any benefits of an imposed CR on lifespan. Male and female Ames dwarf mice and their normal counterparts have been fed ad libitum (AL) or a 30% CR diet for 25-29 months. Animals were monitored daily and weighed weekly. At 12-15 months of age, CR mice weighed significantly less than their AL fed counterparts (normal females: -42%, normal males: -23%, dwarf females: -18.8%, and dwarf males: -22.2%). Only in dwarf females has this significant difference disappeared with age. At one year of age, a comparison of daily food consumption revealed that female dwarf mice consume significantly more food per gram body weight than normal females and a similar tendency is evident for males. Although they received 30% less food, CR mice ate the same amount as AL mice per gram body weight. On measures of total locomotor activity, CR mice were significantly more active than their AL-fed counterparts. On an inhibitory avoidance learning task, 18-21 month old dwarf mice exhibited significantly better retention than their age-and diet-matched normal counterparts. Histopathological analysis in aging dwarf versus normal mice suggested that the incidence of tumors does not differ between the two groups but tumors appear to develop later in dwarf than in normal mice. After 2.25 years on the study 27% of AL normals, 52% of CR normals, 74% of AL dwarfs, and 87% of CR dwarfs are still alive. We conclude that Ames dwarfs are not CR mimetics although they share many characteristics. It remains to be determined whether CR will delay aging and cause a further life extension in Ames dwarf mice.</p>","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"23 1","pages":"9-16"},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-000-0002-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31466272","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":"Membership directory","authors":"D. Curb","doi":"10.1007/s11357-002-0025-9","DOIUrl":"https://doi.org/10.1007/s11357-002-0025-9","url":null,"abstract":"","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"251-281"},"PeriodicalIF":0.0,"publicationDate":"1972-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0025-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52978834","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":"Research fund","authors":"A. Balin","doi":"10.1007/s11357-002-0021-0","DOIUrl":"https://doi.org/10.1007/s11357-002-0021-0","url":null,"abstract":"","PeriodicalId":89818,"journal":{"name":"Journal of the American Aging Association","volume":"25 1","pages":"213-214"},"PeriodicalIF":0.0,"publicationDate":"1954-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11357-002-0021-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"52978785","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}