Volume 6, Issue 2

Leptin and Aging

Beatrice M. Filippi, Tony K.T. Lam,

https://doi.org/10.18632/aging.100637 pp 82—83

PDF How to Cite Request Reprint

Cite this Article

How to cite

Filippi BM, Lam TK, . Leptin and Aging. . 6:82-83. https://doi.org/10.18632/aging.100637

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Evolution of sexually dimorphic longevity in humans

David Gems,

https://doi.org/10.18632/aging.100640 pp 84—91

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gems D, . Evolution of sexually dimorphic longevity in humans. . 6:84-91. https://doi.org/10.18632/aging.100640

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gems, David 
                TI  - Evolution of sexually dimorphic longevity in humans
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100640
                DO  - 10.18632/aging.100640
                SP  - 84
                EP  - 91
                PY  - 
                AB  - Why do humans live longer than other higher primates? Why do women live longer than men? What is the significance of the menopause? Answers to these questions may be sought by reference to the mechanisms by which human aging might have evolved. Here, an evolutionary hypothesis is presented that could answer all three questions, based on the following suppositions. First, that the evolution of increased human longevity was driven by increased late-life reproduction by men in polygynous primordial societies. Second, that the lack of a corresponding increase in female reproductive lifespan reflects evolutionary constraint on late-life oocyte production. Third, that antagonistic pleiotropy acting on androgen-generated secondary sexual characteristics in men increased reproductive success earlier in life, but shortened lifespan. That the gender gap in aging is attributable to androgens appears more likely given a recent report of exceptional longevity in eunuchs. Yet androgen depletion therapy, now used to treat prostatic hyperplasia, appears to accelerate other aspects of aging (e.g. cardiovascular disease). One possibility is that low levels of androgens throughout life reduces aging rate, but late-life androgen depletion does not
                ER  -

Click to copy this citation from the text box above or download the citation:

Hypothalamic-mediated control of glucose balance in the presence and absence of insulin

Teppei Fujikawa, Roberto Coppari,

https://doi.org/10.18632/aging.100641 pp 92—97

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Fujikawa T, Coppari R, . Hypothalamic-mediated control of glucose balance in the presence and absence of insulin. . 6:92-97. https://doi.org/10.18632/aging.100641

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Fujikawa, Teppei 
                AU  - Coppari, Roberto 
                TI  - Hypothalamic-mediated control of glucose balance in the presence and absence of insulin
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100641
                DO  - 10.18632/aging.100641
                SP  - 92
                EP  - 97
                PY  - 
                AB  - Diabetes afflicts hundreds of millions worldwide. People affected by type 1 diabetes mellitus (T1DM; the insulin-deficient form of diabetes) or type 2 diabetes mellitus (T2DM; the insulin-resistant form of diabetes) have significantly reduced life expectancy compared to normal individuals. This is due in part to the fact that (despite improvements) current anti-diabetic approaches are suboptimal. Indeed, severe morbidities (e.g.: cardiovascular disease, hypertension) are still too often associated with diabetes. Recent preclinical results indicate that different types of hypothalamic neurons are endowed with the ability to mediate the hyperglycemia-lowering action of the adipocyte-derived hormone leptin in an insulin-dependent and insulin-independent fashion. These results may pave the way for better anti-diabetic approaches and therefore positively impact on life expectancy of diabetic subjects
                ER  -

Click to copy this citation from the text box above or download the citation:

MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in C. elegans

Michèle Riesen, Inna Feyst, Nattaphong Rattanavirotkul, Marina Ezcurra, Jennifer M.A. Tullet, Irene Papatheodorou, Matthias Ziehm, Catherine Au, Ann F. Gilliat, Josephine Hellberg, Janet M. Thornton, David Gems,

https://doi.org/10.18632/aging.100638 pp 98—117

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Riesen M, Feyst I, Rattanavirotkul N, Ezcurra M, Tullet JM, Papatheodorou I, Ziehm M, Au C, Gilliat AF, Hellberg J, Thornton JM, Gems D, . MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in C. elegans. . 6:98-117. https://doi.org/10.18632/aging.100638

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Riesen, Michèle 
                AU  - Feyst, Inna 
                AU  - Rattanavirotkul, Nattaphong 
                AU  - Ezcurra, Marina 
                AU  - Tullet, Jennifer M.A. 
                AU  - Papatheodorou, Irene 
                AU  - Ziehm, Matthias 
                AU  - Au, Catherine 
                AU  - Gilliat, Ann F. 
                AU  - Hellberg, Josephine 
                AU  - Thornton, Janet M. 
                AU  - Gems, David 
                TI  - MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in <i>C. elegans</i>
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100638
                DO  - 10.18632/aging.100638
                SP  - 98
                EP  - 117
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Riesen, Michèle 
                AU  - Feyst, Inna 
                AU  - Rattanavirotkul, Nattaphong 
                AU  - Ezcurra, Marina 
                AU  - Tullet, Jennifer M.A. 
                AU  - Papatheodorou, Irene 
                AU  - Ziehm, Matthias 
                AU  - Au, Catherine 
                AU  - Gilliat, Ann F. 
                AU  - Hellberg, Josephine 
                AU  - Thornton, Janet M. 
                AU  - Gems, David 
                TI  - MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in <i>C. elegans</i>
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100638
                DO  - 10.18632/aging.100638
                SP  - 98
                EP  - 117
                PY  - 
                AB  - In C. elegans, increased lifespan in daf-2 insulin/IGF-1 receptor mutants is accompanied by up-regulation of the MDL-1 Mad basic helix-loop-helix leucine zipper transcription factor. Here we describe the role of mdl-1 in C. elegans germline proliferation and aging. The deletion allele mdl-1(tm311) shortened lifespan, and did so significantly more so in long-lived daf-2 mutants implying that mdl-1(+) contributes to effects of daf-2 on lifespan. mdl-1 mutant hermaphrodites also lay increased numbers of unfertilized oocytes. During aging, unfertilized oocytes in the uterus develop into tumors, whose development was accelerated by mdl-1(tm311). Opposite phenotypes were seen in daf-2 mutants, i.e. mdl-1 and daf-2 mutant germlines are hyperplastic and hypoplastic, respectively. Thus, MDL-1, like its mammalian orthologs, is an inhibitor of cell proliferation and growth that slows progression of an age-related pathology in C. elegans (uterine tumors). In addition, intestine-limited rescue of mdl-1 increased lifespan but not to wild type levels. Thus, mdl-1 likely acts both in the intestine and the germline to influence age-related mortality.
                ER  -

Click to copy this citation from the text box above or download the citation:

Age-dependent changes in mitochondrial morphology and volume are not predictors of lifespan

Saroj G. Regmi, Stéphane G. Rolland, Barbara Conradt,

https://doi.org/10.18632/aging.100639 pp 118—130

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Regmi SG, Rolland SG, Conradt B, . Age-dependent changes in mitochondrial morphology and volume are not predictors of lifespan. . 6:118-130. https://doi.org/10.18632/aging.100639

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Regmi, Saroj G. 
                AU  - Rolland, Stéphane G. 
                AU  - Conradt, Barbara 
                TI  - Age-dependent changes in mitochondrial morphology and volume are not predictors of lifespan
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100639
                DO  - 10.18632/aging.100639
                SP  - 118
                EP  - 130
                PY  - 
                AB  - Mitochondrial dysfunction is a hallmark of skeletal muscle degeneration during aging. One mechanism through which mitochondrial dysfunction can be caused is through changes in mitochondrial morphology. To determine the role of mitochondrial morphology changes in age-dependent mitochondrial dysfunction, we studied mitochondrial morphology in body wall muscles of the nematode C. elegans. We found that in this tissue, animals display a tubular mitochondrial network, which fragments with increasing age. This fragmentation is accompanied by a decrease in mitochondrial volume. Mitochondrial fragmentation and volume loss occur faster under conditions that shorten lifespan and occur slower under conditions that increase lifespan. However, neither mitochondrial morphology nor mitochondrial volume of five- and seven-day old wild-type animals can be used to predict individual lifespan. Our results indicate that while mitochondria in body wall muscles undergo age-dependent fragmentation and a loss in volume, these changes are not the cause of aging but rather a consequence of the aging process.
                ER  -

Click to copy this citation from the text box above or download the citation:

Reduced bioenergetics and toll-like receptor 1 function in human polymorphonuclear leukocytes in aging

Feng Qian, Xiuyang Guo, Xiaomei Wang, Xiaoling Yuan, Shu Chen, Stephen E. Malawista, Linda K. Bockenstedt, Heather G. Allore, Ruth R. Montgomery,

https://doi.org/10.18632/aging.100642 pp 131—139

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Qian F, Guo X, Wang X, Yuan X, Chen S, Malawista SE, Bockenstedt LK, Allore HG, Montgomery RR, . Reduced bioenergetics and toll-like receptor 1 function in human polymorphonuclear leukocytes in aging. . 6:131-139. https://doi.org/10.18632/aging.100642

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Qian, Feng 
                AU  - Guo, Xiuyang 
                AU  - Wang, Xiaomei 
                AU  - Yuan, Xiaoling 
                AU  - Chen, Shu 
                AU  - Malawista, Stephen E. 
                AU  - Bockenstedt, Linda K. 
                AU  - Allore, Heather G. 
                AU  - Montgomery, Ruth R. 
                TI  - Reduced bioenergetics and toll-like receptor 1 function in human polymorphonuclear leukocytes in aging
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100642
                DO  - 10.18632/aging.100642
                SP  - 131
                EP  - 139
                PY  - 
                AB  - Aging is associated with a progressive decline in immune function (immunosenescence) resulting in an increased susceptibility to viral and bacterial infections. Here we show reduced expression of Toll-like receptor 1 (TLR1) in polymorphonuclear leukocytes (PMN) and an underlying age-dependent deficiency in PMN bioenergetics. In older (&gt;65 years) adults, stimulation through TLR1 led to lower activation of integrins (CD11b and CD18), lower production of the chemokine IL-8, and lower levels of the phosphorylated signaling intermediate p38 MAP kinase than in PMN from younger donors (21-30 years). In addition, loss of CD62L, a marker of PMN activation, was reduced in PMN of older adults stimulated through multiple pathways. Rescue of PMN from apoptosis by stimulation with TLR1 was reduced in PMN from older adults. In seeking an explanation for effects of aging across multiple pathways, we examined PMN energy utilization and found that glucose uptake after stimulation through TLR1 was dramatically lower in PMN of older adults. Our results demonstrate a reduction in TLR1 expression and TLR1-mediated responses in PMN with aging, and reduced efficiency of bioenergetics in PMN. These changes likely contribute to reduced PMN efficiency in aging through multiple aspects of PMN function and suggest potential therapeutic opportunities.
                ER  -

Click to copy this citation from the text box above or download the citation:

Antioxidant SkQ1 delays sarcopenia-associated damage of mitochondrial ultrastructure

Valeriya B. Vays, Chupalav M. Eldarov, Irina M. Vangely, Nataliya G. Kolosova, Lora E. Bakeeva, Vladimir P. Skulachev,

https://doi.org/10.18632/aging.100636 pp 140—148

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Vays VB, Eldarov CM, Vangely IM, Kolosova NG, Bakeeva LE, Skulachev VP, . Antioxidant SkQ1 delays sarcopenia-associated damage of mitochondrial ultrastructure. . 6:140-148. https://doi.org/10.18632/aging.100636

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Vays, Valeriya B. 
                AU  - Eldarov, Chupalav M. 
                AU  - Vangely, Irina M. 
                AU  - Kolosova, Nataliya G. 
                AU  - Bakeeva, Lora E. 
                AU  - Skulachev, Vladimir P. 
                TI  - Antioxidant SkQ1 delays sarcopenia-associated damage of mitochondrial ultrastructure
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100636
                DO  - 10.18632/aging.100636
                SP  - 140
                EP  - 148
                PY  - 
                AB  - A comparative electron-microscopic study of ultrastructure of mitochondria in skeletal muscles of the 3- and 24-month-old Wistar and OXYS rats revealed age-dependent changes in both general organization of the mitochondrial reticulum and ultrastructure of mitochondria. The most pronounced ultrastructure changes were detected in the OXYS rats suffering from permanent oxidative stress. In the OXYS rats, significant changes in mitochondrial ultrastructure were detected already at the age of 3 months. Among them, there were the appearance of megamitochondria and reduction of cristae resulting in formation of cristae-free regions inside mitochondria. In the 24-month-old OXYS rats, mitochondrial reticulum was completely destroyed. In the isotropic region of muscle fiber, only small solitary mitochondria were present. There appeared regions of lysed myofibrils as well as vast regions filled with autophagosomes. A mitochondrial antioxidant SkQ1 (given to rats with food daily in the dose of 250 nmol/kg of body weight for 5 months beginning from the age of 19 months) prevented development of age-dependent destructive changes in both the Wistar and OXYS rats.
                ER  -

Click to copy this citation from the text box above or download the citation:

Multiple dietary supplements do not affect metabolic and cardiovascular health

Andreea Soare, Edward P. Weiss, John O. Holloszy, Luigi Fontana,

https://doi.org/10.18632/aging.100597 pp 149—157

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Soare A, Weiss EP, Holloszy JO, Fontana L, . Multiple dietary supplements do not affect metabolic and cardiovascular health. . 6:149-157. https://doi.org/10.18632/aging.100597

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Soare, Andreea 
                AU  - Weiss, Edward P. 
                AU  - Holloszy, John O. 
                AU  - Fontana, Luigi 
                TI  - Multiple dietary supplements do not affect metabolic and cardiovascular health
                JO  - 
                JA  - 
                VL  - 6
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100597
                DO  - 10.18632/aging.100597
                SP  - 149
                EP  - 157
                PY  - 
                AB  - Dietary supplements are widely used for health purposes. However, little is known about the metabolic and cardiovascular effects of combinations of popular over-the-counter supplements, each of which has been shown to have anti-oxidant, anti-inflammatory and pro-longevity properties in cell culture or animal studies. This study was a 6-month randomized, single-blind controlled trial, in which 56 non-obese (BMI 21.0-29.9 kg/m2) men and women, aged 38 to 55 yr, were assigned to a dietary supplement (SUP) group or control (CON) group, with a 6-month follow-up. The SUP group took 10 dietary supplements each day (100 mg of resveratrol, a complex of 800 mg each of green, black, and white tea extract, 250 mg of pomegranate extract, 650 mg of quercetin, 500 mg of acetyl-l-carnitine, 600 mg of lipoic acid, 900 mg of curcumin, 1 g of sesamin, 1.7 g of cinnamon bark extract, and 1.0 g fish oil). Both the SUP and CON groups took a daily multivitamin/mineral supplement. The main outcome measures were arterial stiffness, endothelial function, biomarkers of inflammation and oxidative stress, and cardiometabolic risk factors. Twenty-four weeks of daily supplementation with 10 dietary supplements did not affect arterial stiffness or endothelial function in nonobese individuals. These compounds also did not alter body fat measured by DEXA, blood pressure, plasma lipids, glucose, insulin, IGF-1, and markers of inflammation and oxidative stress. In summary, supplementation with a combination of popular dietary supplements has no cardiovascular or metabolic effects in non-obese relatively healthy individuals.
                ER  -

Click to copy this citation from the text box above or download the citation:

Volume 6, Issue 2

Editorial

Leptin and Aging

Beatrice M. Filippi, Tony K.T. Lam,

Review

Evolution of sexually dimorphic longevity in humans

David Gems,

Research Perspective

Hypothalamic-mediated control of glucose balance in the presence and absence of insulin

Teppei Fujikawa, Roberto Coppari,

Research Papers

MDL-1, a growth- and tumor-suppressor, slows aging and prevents germline hyperplasia and hypertrophy in C. elegans

Michèle Riesen, Inna Feyst, Nattaphong Rattanavirotkul, Marina Ezcurra, Jennifer M.A. Tullet, Irene Papatheodorou, Matthias Ziehm, Catherine Au, Ann F. Gilliat, Josephine Hellberg, Janet M. Thornton, David Gems,

Age-dependent changes in mitochondrial morphology and volume are not predictors of lifespan

Saroj G. Regmi, Stéphane G. Rolland, Barbara Conradt,

Reduced bioenergetics and toll-like receptor 1 function in human polymorphonuclear leukocytes in aging

Feng Qian, Xiuyang Guo, Xiaomei Wang, Xiaoling Yuan, Shu Chen, Stephen E. Malawista, Linda K. Bockenstedt, Heather G. Allore, Ruth R. Montgomery,

Antioxidant SkQ1 delays sarcopenia-associated damage of mitochondrial ultrastructure

Valeriya B. Vays, Chupalav M. Eldarov, Irina M. Vangely, Nataliya G. Kolosova, Lora E. Bakeeva, Vladimir P. Skulachev,

Multiple dietary supplements do not affect metabolic and cardiovascular health

Andreea Soare, Edward P. Weiss, John O. Holloszy, Luigi Fontana,

Explore This Issue