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• Research Paper Volume 13, Issue 21 pp 23936-23952

  Impaired glucose metabolism reduces the neuroprotective action of adipocytokines in cognitively normal older adults with insulin resistance

  Relevance score: 7.091994

  Karel M. Lopez-Vilaret, Jose L. Cantero, Marina Fernandez-Alvarez, Miguel Calero, Olga Calero, Mónica Lindín, Montserrat Zurrón, Fernando Díaz, Mercedes Atienza

  Keywords: adiponectin, leptin, cognitive function, cortical thickness, metabolism

  Published in Aging on November 3, 2021

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  Evidence suggests that aging-related dysfunctions of adipose tissue and metabolic disturbances increase the risk of diabetes and metabolic syndrome (MtbS), eventually leading to cognitive impairment and dementia. However, the neuroprotective role of adipocytokines in this process has not been specifically investigated. The present study aims to identify metabolic alterations that may prevent adipocytokines from exerting their neuroprotective action in normal ageing. We hypothesize that neuroprotection may occur under insulin resistance (IR) conditions as long as there are no other metabolic alterations that indirectly impair the action of adipocytokines, such as hyperglycemia. This hypothesis was tested in 239 cognitively normal older adults (149 females) aged 52 to 87 years (67.4 ± 5.9 yr). We assessed whether the homeostasis model assessment-estimated insulin resistance (HOMA-IR) and the presence of different components of MtbS moderated the association of plasma adipocytokines (i.e., adiponectin, leptin and the adiponectin to leptin [Ad/L] ratio) with cognitive functioning and cortical thickness. The results showed that HOMA-IR, circulating triglyceride and glucose levels moderated the neuroprotective effect of adipocytokines. In particular, elevated triglyceride levels reduced the beneficial effect of Ad/L ratio on cognitive functioning in insulin-sensitive individuals; whereas under high IR conditions, it was elevated glucose levels that weakened the association of the Ad/L ratio with cognitive functioning and with cortical thickness of prefrontal regions. Taken together, these findings suggest that the neuroprotective action of adipocytokines is conditioned not only by whether cognitively normal older adults are insulin-sensitive or not, but also by the circulating levels of triglycerides and glucose, respectively.

• Research Paper Volume 13, Issue 12 pp 16834-16858

  The consequences of a high-calorie diet background before calorie restriction on skeletal muscles in a mouse model

  Relevance score: 7.1225643

  Martin Maldonado, Jianying Chen, Yang Lujun, Huiqin Duan, Mazhar Ali Raja, Ting Qu, Tianhua Huang, Jiang Gu, Ying Zhong

  Keywords: calorie-intervention, skeletal muscle, sirtuins, mitochondria, adiponectin

  Published in Aging on June 24, 2021

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  The beneficial effects of calorie restriction (CR) are numerous. However, there is no scientific evidence about how a high-calorie diet (HCD) background influences the mechanisms underlying CR on skeletal muscles in an experimental mouse model.

  Herein we present empirical evidence showing significant interactions between HCD (4 months) and CR (3 months).

  Pectoralis major and quadriceps femoris vastus medialis, in the experimental and control groups, displayed metabolic and physiologic heterogeneity and remarkable plasticity, according to the dietary interventions.

  HCD-CR not only altered genetic activation patterns of satellite SC markers but also boosted the expression of myogenic regulatory factors and key activators of mitochondrial biogenesis, which in turn were also associated with metabolic fiber transition.

  Our data prompt us to theorize that the effects of CR may vary according to the physiologic, metabolic, and genetic peculiarities of the skeletal muscle described here and that INTM/IM lipid infiltration and tissue-specific fuel-energy status (demand/supply) both hold dependent-interacting roles with other key anti-aging mechanisms triggered by CR.

  Systematic integration of an HCD with CR appears to bring potential benefits for skeletal muscle function and energy metabolism. However, at this stage of our research, an optimal balance between the two dietary conditions, where anti-aging effects can be accomplished, is under intensive investigation in combination with other tissues and organs at different levels of organization within the organ system.

• Research Paper Volume 13, Issue 11 pp 15433-15443

  Galectin-3/adiponectin as a new biological indicator for assessing the risk of type 2 diabetes: a cross-sectional study in a community population

  Relevance score: 5.903216

  Diaozhu Lin, Xiaosi Hong, Kan Sun, Xiaoyun Zhang, Hong Lian, Jiahuan Wang, Na Mao, Xiuwei Zhang, Meng Ren, Li Yan, Feng Li, Lili You

  Keywords: type 2 diabetes, age, galectin-3/adiponectin, diabetes risk assessment model

  Published in Aging on June 7, 2021

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  Objective: This study aimed to explore the association between the risk of newly diagnosed type 2 diabetes and galectin-3 and adiponectin and to investigate whether their joint action shows a favorable diabetes assessment performance.

  Methods: We conducted a community-based study in 135 newly diagnosed patients with type 2 diabetes and 270 age- and sex-matched nondiabetic patients. Odds ratios and 95% confidence intervals were determined using logistic regression analysis. Receiver operating characteristic curve, decision curve analysis and calibration plot were used to explore their efficacy and clinical utility for models.

  Results: High quartiles of galectin-3/adiponectin (quartile 4 vs 1: OR 2.43 [95% CIs: 1.21–5.00]) showed the strongest correlation with an increased risk of type 2 diabetes in the total population, which was consistent in the older population (age≥50 years old) in adjustment models. The combination + lipids + galectin-3/adiponectin model (AUC = 0.72 [95% CIs: 0.66-0.77]) displayed better diabetes assessment performance than the other two models.

  Conclusions: High galectin-3 and low adiponectin levels were associated with the high risk of diabetes, and their joint action was a superior promising factor for evaluating diabetes risk. The diabetes discriminative strength of galectin-3/adiponectin was better in the older population than the younger.

• Review Volume 12, Issue 5 pp 4660-4672

  Adiponectin in renal fibrosis

  Relevance score: 8.877462

  Huan Jing, Simin Tang, Sen Lin, Meijuan Liao, Hongtao Chen, Youling Fan, Jun Zhou

  Keywords: adiponectin, renal fibrosis

  Published in Aging on February 17, 2020

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  Renal fibrosis is an inevitable consequence of parenchymal scarring and is the common final pathway that mediates almost all progressive renal diseases. Adiponectin, a hormone produced by adipose tissue, possesses potent anti-insulin, anti-inflammatory, and anti-fibrotic properties. Reportedly, adiponectin serves as an important messenger that facilitates complex interactions between adipose tissue and other metabolically related organs. In recent years, a growing body of evidence supports adiponectin involvement in renal fibrosis. These studies provide a deeper understanding of the molecular mechanism of action of adiponectin in renal fibrosis and also offer a potential preventive and therapeutic target for renal fibrosis. In this review, the physiological role of adiponectin is briefly introduced, and then the mechanism of adiponectin-mediated renal fibrosis and the related signaling pathways are described. Finally, we summarize the findings regarding the clinical value of adiponectin in renal fibrotic diseases and prospected its application potential.

  

  The pathomechanism of renal fibrosis involves several factors, including oxidative stress and related inflammation, disturbances of glucose metabolism, and hemodynamic abnormalities. Many studies have confirmed that APN is involved in reducing renal fibrosis, and its specific mechanisms include reducing renal toxicity, reducing renal cell damage, resisting fibrosis, and reducing proteinuria to protect the glomerular filter.

  
  
  

  

  The molecular mechanisms driving renal fibrosis are wide-ranging and complex, among which signaling pathways are very important. The common signaling pathways activated in adiponectin-mediated renal fibrosis are the AMPK and peroxisome proliferators-activated receptors (PPARs) pathway.

  
  
  

  

  Accumulative evidence about the renoprotective role of adiponectin promotes a therapeutic strategy for renal fibrosis targeting adiponectin, such as increasing the plasma adiponectin level or increasing the sensitivity of adiponectin by activating adiponectin receptors. Numerous studies have confirmed that PPAR-γ agonist compounds increase adiponectin secretion and circulating adiponectin levels in adipose tissue. And the exogenous adiponectin is also currently a hot focus for the treatment of kidney disease. In addition, AdipoRon directly activates intrarenal AdipoR1 and AdipoR2, and promotes downstream reactions, thereby restrainting renal fibrosis.

  
  
  

• Research Paper Volume 11, Issue 19 pp 8329-8346

  Involvement of adiponectin in age-related increases in tear production in mice

  Relevance score: 5.515554

  Yosuke Shikama, Mie Kurosawa, Masae Furukawa, Naozumi Ishimaru, Kenji Matsushita

  Keywords: dry eye, adiponectin, peroxisome proliferator-activated receptor gamma, senescence-associated T cells, aging

  Published in Aging on October 8, 2019

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  Common age-related changes in the human eye contribute to the development of dry eye, including decreases in aqueous tear production. Although the infiltration of lymphocytes into the lacrimal glands occurs with age, age-related increases in tear production have also been observed in mice; however, the mechanisms underlying this increase remain unclear. We herein demonstrated that increases in tear production were not dependent on body weight gain or systemic conditions, such as insulin resistance, using aged mice and high-fat diet-fed mice. The results obtained also showed that senescence-associated T (SA-T) cells accumulated in the lacrimal glands of aged mice, particularly females. Expression levels of the nuclear transcription factor peroxisome proliferator-activated receptor-γ (PPARγ) in whole lacrimal glands and epithelial cells isolated from lacrimal glands were significantly higher in aged mice than in young mice. The expression levels of adiponectin and one of its receptors, AdipoR2, also increased in the lacrimal glands of aged mice, but not in those of high-fat diet-fed mice. Collectively, the present results indicate that PPARγ and adiponectin-mediated signaling contribute to age-related increases in tear production in mice and have potential as therapeutic targets for the treatment of dry eye in humans.

  

  Pilocarpine-stimulated tear secretion increased in aged mice, but not in high-fat diet-fed mice. (A and B) Body weights and the weights of the lacrimal glands (LG) in young, middle-aged, and aged mice. Upper and lower graphs show male (N=5) and female mice (N=4-6), respectively. (C–E) Absolute volume of tear flow ©, adjusted by body weight (D) or LG weight (E). Upper and lower graphs show male (N=6) and female mice (N=4-6), respectively. (F) Body weight in normal diet (ND)- or high-fat diet (HFD)-fed mice for the indicated period (N=4). Upper and lower graphs show male and female mice, respectively. (G and H) Absolute volume of tear flow (G) adjusted by body weight (H) in ND or HFD-fed mice for the indicated period (N=4). Upper and lower graphs show male and female mice, respectively. Values are presented as means ± SEM. *p<0.05 and **p<0.01 (an unpaired Student’s t-test). #p<0.05 and ##p<0.01 versus young mice (Dunnett’s multiple comparison test).

  
  
  

  

  Effects of aging or high-fat diet feeding on M3R mRNA expression in lacrimal glands. M3R mRNA expression levels in young and aged mice (N=7-8) (A), and in mice fed a normal diet (ND) or high-fat diet (HFD) for 8 weeks (N=4-5) (B). Values are presented as means ± SEM. NS, not significant (an unpaired Student’s t-test).

  
  
  

  

  SA-T cells accumulate in lacrimal glands of aged mice, particularly in female mice. (A and B) Naïve (CD44^loCD62L^hi) and effector memory (CD44^hiCD62L^lo) expression in CD4⁺ T cells (A), or PD-1⁺CD153⁺ expression in effector memory CD4⁺ T cells (B) in the lacrimal glands of young and aged mice. Results are representative of those from each group of mice. (C and D) Proportions (N=5) (C) and numbers adjusted by the lacrimal gland (LG) weight (N=4) (D) of PD-1⁺CD153⁺ cells gated on effector memory CD4⁺ T cells in the LG of young and aged mice. (E) CD153 mRNA expression levels in the LG of young and aged female mice, and of female mice fed a normal diet (ND) or high-fat diet (HFD) for 8 weeks (N=4-5). Values are presented as means ± SEM. *p<0.05 and **p<0.01 (an unpaired Student’s t-test).

  
  
  

  

  PPARγ expression in lacrimal glands and adiponectin mRNA expression in the white adipose tissue of aged and high-fat diet-fed mice. (A and B) PPARγ mRNA expression levels in the lacrimal glands of young and aged mice (N=7-8) (A), or of mice fed a normal diet (ND) or high-fat diet (HFD) for 8 weeks (N=4-5) (B). (C) PPARγ mRNA expression levels in the epithelial cells of the lacrimal glands of young and aged mice (N=4). (D) Detection of the PPARγ protein by Western blotting. Lysates prepared from the lacrimal glands of young and aged mice were immunoblotted with anti-AdipoR2 and anti-β-Actin antibodies. Left and right images show male (N=2) and female mice (N=2), respectively. The positive control (Posi) is a lysate prepared from the subcutaneous fat of young mice. The bar graph shows integrated signal intensities in AdipoR2 normalized to that of β-Actin (N=4). (E) PPARγ expression in the acinar cells of the lacrimal glands of young and aged mice as detected by immunofluorescence. Nuclei were stained with DAPI. Bars = 10 μm. (F) Adiponectin mRNA expression levels in the mesenteric white adipose tissues of young and aged mice (N=4-5). Values are presented as means ± SEM. NS, not significant. **p<0.01 (an unpaired Student’s t-test).

  
  
  

  

  Influence of aging or high-fat diet feeding on adiponectin, adipoR1, and adipoR2 expression in lacrimal glands. Adiponectin (A), adipoR1 (B), and adipoR2 (C) mRNA expression levels in lacrimal glands. Upper and lower graphs show results in young and aged mice (N=7-8), and in mice fed a normal diet (ND) or high-fat diet (HFD) for 8 weeks (N=4-5), respectively. (D) Detection of the AdipoR2 protein by Western blotting. Lysates prepared from the lacrimal glands of young and aged mice were immunoblotted with anti-AdipoR2 and anti-β-Actin antibodies. Left and right images show male (N=2) and female mice (N=2), respectively. The bar graph shows integrated signal intensities in AdipoR2 normalized to that of β-Actin (N=4). (E) AdipoR2 expression in the lacrimal glands of young and aged mice as detected by immunofluorescence. Nuclei were stained with DAPI. Bars = 40 μm. Values are presented as means ± SEM. NS, not significant. *p<0.05 and **p<0.01 (an unpaired Student’s t-test).

  
  
  

• Research Paper Volume 11, Issue 12 pp 4159-4182

  Proteomics-based identification of different training adaptations of aged skeletal muscle following long-term high-intensity interval and moderate-intensity continuous training in aged rats

  Relevance score: 6.5161424

  Fang-Hui Li, Lei Sun, Da-Shuai Wu, Hao-En Gao, Zhu Min

  Keywords: aging, skeletal muscle, proteome, high-intensity interval training, adiponectin

  Published in Aging on June 26, 2019

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  Aging-associated loss of skeletal muscle mass and force increases the risk of falls, impairs mobility, and leads to a reduced quality of life. High-intensity interval training (HIIT) is superior to moderate-intensity continuous training (MICT) for improving morphological and metabolic adaptations of skeletal muscle in older adults, but the underlying mechanism is unknown. Aged female rats underwent HIIT and MICT for 8 months, and their differential impacts on skeletal muscle proteome were investigated. HIIT resulted in a larger improvement in grip strength and fiber cross-sectional area, with similar increases in inclined plane performance and time to exhaustion. Proteomic analysis showed that common training adaptations of both protocols included changes to muscle contraction, focal adhesion signaling, mitochondrial function, apoptosis and regeneration, and anti-oxidation, whereas protein processing in the endoplasmic reticulum and adipocytokine signaling were specifically altered in the MICT and HIIT groups, respectively. Immunoblotting showed that upregulation of the adiponectin/AMPK signaling pathway may be associated with improvements in autophagy, oxidative stress, mitochondrial function, and apoptosis in aged skeletal muscle following HIIT. Thus, understanding the molecular differences in training adaptations from these two exercise modalities may aid in combatting sarcopenia.

  

  Effect of MICT and HIIT protocols on physical performance and fiber cross sectional area. Changes in time to exhaustion (min) (A), grip strength (N·g^–1) (B), maximum run speed (m·min^-1) (C), inclined plane performance (D), relative gastrocnemius weight (E), absolute gastrocnemius weight (F), muscle fiber morphology (G), mean cross-sectional area (H), and frequency distribution of mean gastrocnemius fiber cross sectional area (I). SED, sedentary control; MICT, moderate-intensity continuous training; HIIT, high-intensity interval training; BW, body weight. Data were analyzed by one-way ANOVA followed by Tukey’s post-hoc test and are presented as mean ± SD. ^* p < 0.05 vs. SED; ^** p < 0.01 vs. SED; ^# p < 0.05 vs. MICT.

  
  
  

  

  Relative protein abundances in the red gastrocnemius muscle of rats in the MICT, HIIT, and SED groups. (A) Heat map and (B) volcano plot of significantly up- and downregulated proteins in the red gastrocnemius muscle from MICT and SED rats (p < 0.05, fold change > ± 1.5). (C) Heat map and (D) volcano plot of significantly up- and downregulated proteins in the red gastrocnemius muscle from HIIT and SED rats. (E) Overlap of proteins up- and downregulated following different modes of exercise training compared with their levels in the SED group.

  
  
  

  

  Evaluation of mRNA levels following HIIT and MICT. SED, sedentary; MICT, moderate-intensity continuous training; HIIT, high-intensity interval training; DnaJ heat shock protein family (Hsp40) member A2, Dnaja2; Superoxide dismutase 2, Sod2; Junctophilin 1, Jph1; Synaptophysin-like 2, Sypl2; Forkhead box O 1, FOXO1. Data were analyzed by one-way ANOVA followed by Tukey’s post-hoc test and are reported as the mean ± SD. ^* p < 0.05 vs. SED; ^** p < 0.01 vs. SED; ^# p < 0.05 vs. MICT.

  
  
  

  

  Expression of autophagy (A), apoptosis (B), and mitochondrial function markers (C), and adipocytokine signaling-related proteins (D). SED, sedentary; MICT, moderate-intensity continuous training; HIIT, high-intensity interval training; succinate dehydrogenase, SDH; sirtuin 3, SIRT3; aldehyde dehydrogenase 2, ALDH2; peroxisome proliferator-activated receptor γ coactivator-1Α, PGC-1a; adiponectin, ADP; autophagy-related gene-3, Atg-3; microtubule-associated protein 1 light chain 3 II, LC3-II; B-cell lymphoma 2, Bcl-2; Bcl-2-associated X protein, Bax; AMP-activated protein kinase, AMPK; adiponectin receptor 1, ADPR1; Forkhead box O1, FOXO1. Data were analyzed by one-way ANOVA followed by Tukey’s post-hoc and are presented as mean ± SD. ^* p < 0.05 vs. SED; ^** p < 0.01 vs. SED; ^# p < 0.05 vs. MICT; ^## p < 0.01 vs. MICT.

  
  
  

  

  Proposed model of the mechanism by which HIIT improved skeletal muscle function in aged rats. HIIT protocols preserve skeletal muscle function by activating lysosomal degradation and improving mitochondrial OXPHOS via the ADP/ADPR1 axis, mediated by the AMPK pathway.

  
  
  

• Research Paper Volume 10, Issue 3 pp 386-401

  Metformin reduces glucose intolerance caused by rapamycin treatment in genetically heterogeneous female mice

  Relevance score: 7.6818542

  Roxanne Weiss, Elizabeth Fernandez, Yuhong Liu, Randy Strong, Adam B. Salmon

  Keywords: mTOR, gluconeogenesis, AMPK, leptin, adiponectin, interventions, insulin

  Published in Aging on March 22, 2018

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  The use of rapamycin to extend lifespan and delay age-related disease in mice is well-established despite its potential to impair glucose metabolism which is driven partially due to increased hepatic gluconeogenesis. We tested whether a combination therapeutic approach using rapamycin and metformin could diminish some of the known metabolic defects caused by rapamycin treatment in mice. In genetically heterogeneous HET3 mice, we found that chronic administration of encapsulated rapamycin by diet caused a measurable defect in glucose metabolism in both male and female mice as early as 1 month after treatment. In female mice, this defect was alleviated over time by simultaneous treatment with metformin, also by diet, such that females treated with both drugs where indistinguishable from control mice during glucose tolerance tests. While rapamycin-mediated glucose intolerance was unaffected by metformin in males, we found metformin prevented rapamycin-mediated reduction in insulin and leptin concentrations following 9 months of co-treatment. Recently, the Interventions Testing Program showed that mice treated with metformin and rapamycin live at least as long as those treated with rapamycin alone. Together, our data provide compelling evidence that the pro-longevity effects of rapamycin can be uncoupled from its detrimental effects on metabolism through combined therapeutic approaches.

  

  Metformin prevents rapamycin-induced weight loss in male mice. Body weights over time for (A) male and (B) female HET3 mice fed control (open square) diet or diets containing metformin (open circle), rapamycin (closed square), or both metformin and rapamycin (closed circle). Symbols represent mean values at indicated time point ± SEM. For all groups, n=10. Letters indicate significant difference among groups.

  
  
  

  

  Metformin abrogates rapamycin-mediated glucose intolerance in female mice. Glucose tolerance tests performed in male (left) and female (right) mice following (A) 1, (B) 2, (C) 3, or (D) 9 months of indicated diet treatments. Symbols represent mean values for indicated group at each time point ± SEM. For all groups, n=8-10.

  
  
  

  

  Combined effects of rapamycin and metformin on glucose metabolism. (A) Area under the curve for glucose tolerance tests repeated in the same cohort of animals following indicated months of treatment. Symbols represent mean values for indicated group at each time point ± SEM. (B) Area under the curve calculated for insulin tolerance tests performed following 3 months of treatment. Bars represent mean values for indicated group at each time point ± SEM. (C) Insulin concentration in plasma collected from fed mice following 9 months of treatment on the indicated diets. Bars represent mean values for indicated group at each time point ± SEM. For glucose and insulin tolerance test, n=8-10 for all groups. For insulin measurements, n=8-10 for all groups.

  
  
  

  

  Rapamycin and metformin effects on circulating metabolic markers. (A) Triglycerides, (B) Adiponectin and (C) Leptin in plasma collected from fed mice following 9 months of treatment on the indicated diets. For A-C, n=8-10 for all groups. Rapamycin and metformin effects on hepatic gluconeogenesis. (D) relative phosphoenolpyruvate carboxykinase (PEPCK) expression and (E) relative glucose 6-phosphatase (G6P) expression in liver from male and female mice fed indicated diets. For D and E, n = 5 for all groups. For all, bars represent mean values for indicated group ± SEM.

  
  
  

  

  No effect of metformin on rapamycin-mediated mTORC1 inhibition. Quantification of phosphorylation/total protein ratios for S6 (left) and Akt (right) for liver, adipose tissue and muscle collected from male (A) and female (B) mice. Bars represent mean values for indicated diet/sex ± SEM. For all groups, n=6.

  
  
  

  

  Mild activation of AMPK signaling in metformin treated mice. Quantification of phosphorylation/total protein ratios for (A) AMPKα and (B) ACC from liver of male and female mice fed indicated diets. Bars represent mean values for diet/sex ± SEM. For all groups, n=6.

  
  
  

• Research Paper Volume 6, Issue 10 pp 900-912

  The effect of calorie restriction on insulin signaling in skeletal muscle and adipose tissue of Ames dwarf mice

  Relevance score: 6.44165

  Denise S. Wiesenborn, Vinal Menon, Xu Zhi, Andrew Do, Adam Gesing, Zhihui Wang, Andrzej Bartke, Deborah A. Altomare, Michal M. Masternak

  Keywords: Ames dwarf, insulin, adipose tissue, skeletal muscle, adiponectin, obesity

  Published in Aging on October 5, 2014

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  Long-living Ames dwarf (df/df) mice are homozygous for a mutation of the Prop1^df gene. As a result, mice are deficient in growth hormone (GH), prolactin (PRL) and thyrotropin (TSH). In spite of the hormonal deficiencies, df/df mice live significantly longer and healthier lives compared to their wild type siblings. We studied the effects of calorie restriction (CR) on the expression of insulin signaling genes in skeletal muscle and adipose tissue of normal and df/df mice. The analysis of genes expression showed that CR differentially affects the insulin signaling pathway in these insulin target organs. Moreover, results obtained in both normal and Ames dwarf mice indicate more direct effects of CR on insulin signaling genes in adipose tissue than in skeletal muscle. Interestingly, CR reduced the protein levels of adiponectin in the epididymal adipose tissue of normal and Ames dwarf mice, while elevating adiponectin levels in skeletal muscle and plasma of normal mice only.

  In conclusion, our findings suggest that both skeletal muscle and adipose tissue are important mediators of insulin effects on longevity. Additionally, the results revealed divergent effects of CR on expression of genes in the insulin signaling pathway of normal and Ames dwarf mice.

  

  The effect of CR on bodyweight (A) and fasting blood glucose (B) of Normal (N) and Ames dwarf (df/df) mice fed ad libitum (AL) or subjected to 30% calorie restriction (CR). Groups which do not share the same letter display a statistical significance (p < 0.05).

  
  
  

  

  Relative gene expression in skeletal muscle of Normal (N) and Ames dwarf (df/df) mice fed ad libitum (AL) or subjected to 30% calorie restriction (CR). Groups which do not share the same letter display a statistical significance (p < 0.05).

  
  
  

  

  Relative gene expression in epididymal adipose tissue of Normal (N) and Ames dwarf (df/df) mice fed ad libitum (AL) or subjected to 30% calorie restriction (CR). Groups which do not share the same letter display a statistical significance (p < 0.05)

  
  
  

  

  Adiponectin levels in Normal (N) and Ames dwarf (df/df) mice fed ad libitum (AL) or subjected to 30% calorie restriction (CR). (A) Plasma adiponcetin, (B) mRNA adiponectin in epididymal adipose tissue, (C) Protein level of adiponectin in epididymal adipose tissue, (D) mRNa adiponectin in skeletal muscle, (E) protein level of adiponectin in skeletal muscle. Groups which do not share the same letter display a statistical significance (p < 0.05).

  
  
  

  

  Adipocytes of epididymal adipose tissue from Normal and Ames dwarf mice. Histological effect of genotype and CR on adipocytes size of epididymal adipose tissue from ormal and Ames dwarf mice.

  
  
  

• Research Paper pp undefined-undefined

  Adiponectin is associated with inflammaging and age-related salivary gland lipid accumulation

  Relevance score: 7.4624553

  Ji Won Kim, Jeong Mi Kim, Mi Eun Choi, Eun Jeong Jeon, Jin-Mi Park, Young-Mo Kim, Jeong-Seok Choi

  Keywords: adiponectin, inflammation, aging, salivary gland, lipid

  Published in Aging on Invalid Date

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  Dry mouth is frequently observed in the elderly, and enhanced lipid accumulation plays a critical role in cellular senescence in the salivary gland (SG). We investigated the mechanisms that mediate lipogenesis-associated SG senescence. Adult (28.6 ± 6.6 y.o. and 43.3 ± 1.5 y.o.) and aged (82.0 ± 4.3 y.o. and 88.0 ± 4.3 y.o.) human parotid and submandibular glands were compared with respect to histologic findings, 8-OHdG (8-hydroxy 2 deoxyguanosine) expression patterns, TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) and SA-β-gal (senescence-associated β-galactosidase) assay results. Also, microarray analysis was performed on RNA extracted from adult and aged SG to identify DEGs (differentially expressed genes). The effects of silencing ADIPOQ (Adiponectin) were evaluated by quantifying cell proliferation, immunohistochemical staining for cellular senescence and inflammation-associated proteins, SA-β-gal assays, RT-PCR, and western blot. Histological findings demonstrated the presence of more lipocytes, chronic inflammation, fibrosis, and lymphocytic infiltration in old SG. In addition, old tissues demonstrated higher expressions of SA-β-gal, more apoptotic cells in TUNEL assays, and higher oxidative stress by 8-OHdG immunostaining. Microarray analysis showed lipogenesis was significantly upregulated in old tissues. Silencing of ADIPOQ (a lipogenesis-related gene) reduced inflammation and SA-β-gal levels and increased cell proliferation and the expressions of amylase and aquaporin 5 in human SG epithelial cells. The study shows ADIPOQ is a potential target molecule for the modulation of lipogenesis associated with SG senescence.