scholarly journals Protective Effects of N1-Methylnicotinamide Against High-Fat Diet- and Age-Induced Hearing Loss via Moderate Overexpression of Sirtuin 1 Protein

2021 ◽  
Vol 15 ◽  
Author(s):  
Toru Miwa
Keyword(s):  
Hearing Loss ◽  
High Fat Diet ◽  
Sirtuin 1 ◽  
Mrna Levels ◽  
Protective Effects ◽  
High Fat ◽  
Protein Levels ◽  
Low Fat Diet ◽  
Age Related ◽  
Cochlear Morphology

Age-related hearing loss (ARHL) is the most common form of hearing loss and the predominant neurodegenerative disease associated with aging. Sirtuin 1 (SIRT1) is associated with the most complex physiological processes, including metabolism, cancer onset, and aging. SIRT1 protein levels are enhanced by the conversion of nicotinamide to N1-methylnicotinamide (MNAM), independent of its mRNA levels. Moreover, MNAM has implications in increased longevity achieved through its mitohormetic effects. Nicotinamide N-methyltransferase (Nnmt) is an enzyme involved in MNAM metabolism, and its level increases under caloric restriction (CR) conditions. The CR condition has implications in delaying ARHL onset. In this study, we aimed to determine the relationship between diet, hearing function, SIRT1 and SIRT3 expression levels in the inner ear, and cochlear morphology. Mice fed with a high-fat diet (HFD), HFD + 1% MNAM, and low-fat diet (LFD) were monitored for age-related auditory-evoked brainstem responses, and changes in cochlear histology, metabolism, and protein and mRNA expressions were analyzed. Our results revealed that the HFD- and aging-mediated downregulated expression of SIRT1 and SIRT3 promoted hearing loss that was obfuscated by MNAM supplementation-induced upregulated expression of cochlear SIRT1 and SIRT3. Thus, our results suggest that MNAM can be used as a therapeutic agent for preventing ARHL.

scholarly journals Resveratrol Supplementation Attenuates Cognitive and Molecular Alterations Under Maternal High-Fat Diet Intake: Multigenerational Epigenetic Inheritance.

2020 ◽  
Author(s):  
Vanesa Izquierdo ◽  
Verónica Palomera-Ávalos ◽  
Mercè Pallàs ◽  
Christian Griñán-Ferré
Keyword(s):  
Gene Expression ◽  
Cognitive Decline ◽  
High Fat Diet ◽  
Epigenetic Inheritance ◽  
Adult Offspring ◽  
High Fat ◽  
Molecular Alterations ◽  
Protein Levels ◽  
Age Related ◽  
Inflammatory Profile

Environmental factors as maternal high-fat diet (HFD) intake can increase the risk of age-related cognitive decline in adult offspring. The epigenetic mechanisms are a possible link between diet effect and neurodegeneration across generations. Here, we found a significant decrease in triglyceride levels in a high-fat diet with resveratrol HFD+RV group and the offspring. Firstly, we obtained better cognitive performance in HFD+RV groups and their offspring. Molecularly, a significant increase in 5-mC levels, as well as increased gene expression of Dnmt1 and Dnmt3a in HFD+RV F1 group, were found. Furthermore, a significantly increased of m6A levels in HFD+RV F1 were found, and there were changes in gene expression of its enzymes (Mettl3 and Fto). Moreover, we found a decrease in gene expression levels of pro-inflammatory markers such as Il1-β, Il-6, Tnf-α, Cxcl-10, Mcp-1 and Tgf-β1 in HFD+RV and HFD+RV F1 groups. Moreover, there was increased gene expression of neurotrophins such as Ngf and Nt3 and its receptors TrkA and TrkB. Likewise, an increase in protein levels of BDNF and p-Akt in HFD+RV F1 was found. These results suggest that maternal RV supplementation under HFD intake prevents cognitive decline in SAMP8 adult offspring, promoting a reduction in triglycerides and leptin plasma levels, changes in the pro-inflammatory profile, restoring the epigenetic landscape as well as synaptic plasticity.

scholarly journals Time-Restricted Feeding Restores Obesity-Induced Alteration in Adipose Tissue Immune Cell Phenotype

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3780
Author(s):  
Youngyoon Lee ◽  
Yelim Kim ◽  
Minam Lee ◽  
Dayong Wu ◽  
Munkyong Pae
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
High Fat Diet ◽  
Immune Cell ◽  
Cell Phenotype ◽  
Mrna Levels ◽  
Restricted Feeding ◽  
High Fat ◽  
Low Fat Diet ◽  
Adipose Tissue Macrophages

Studies suggest that time-restricted feeding (TRF) may prevent obesity and its commodities. At present, little is known about how TRF impacts immune cells, and whether such an effect is linked to altered metabolic parameters under condition of a high-fat diet (HFD)-induced obesity. To address these issues, we conducted a study in which we determined whether TRF has therapeutic efficacy against weight gain, adiposity, as well as associated immune cell disturbance found in obese mice. Six-week-old male C57BL/6 mice were fed a low-fat diet (LFD) or HFD ad libitum for six weeks, after which time a subgroup of HFD mice was switched to the 10 h TRF paradigm (HFD-TRF) for additional eight weeks. We found that TRF intervention reduced HFD-induced weight gain. Even with comparable fat mass and mean adipocyte area, the HFD-TRF group had lower mRNA levels of proinflammatory cytokine Tnfα and chemokine Ccl8, along with reduced numbers of adipose tissue macrophages (ATM), CD11c+ ATM, and CD8+ T cell compared to the HFD group, while maintaining CD8+ to CD4+ ratio at levels similar to those in the LFD group. Furthermore, TRF intervention was effective in improving glucose tolerance and reducing HOMA-IR. Taken together, our findings suggest that TRF restores the obesity-induced alteration in immune cell composition, and this effect may in part contribute to health benefits (including insulin sensitivity) of practicing TRF.

scholarly journals A High-Fat Diet Delays Age-Related Hearing Loss Progression in C57BL/6J Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (1) ◽  
pp. e0117547 ◽  
Author(s):  
Takeshi Fujita ◽  
Daisuke Yamashita ◽  
Natsumi Uehara ◽  
Go Inokuchi ◽  
Shingo Hasegawa ◽  
...  
Keyword(s):  
Hearing Loss ◽  
High Fat Diet ◽  
High Fat ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals Hypothalamic PDE3B deficiency alters body weight and glucose homeostasis in mouse

2018 ◽  
Vol 239 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Maitrayee Sahu ◽  
Prashanth Anamthathmakula ◽  
Abhiram Sahu
Keyword(s):  
Body Weight ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Specific Response ◽  
Mrna Levels ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Phosphodiesterase 3B

Pharmacological studies have suggested hypothalamic phosphodiesterase-3B to mediate leptin and insulin action in regulation of energy homeostasis. Whereas Pde3b-null mice show altered energy homeostasis, it is unknown whether this is due to ablation of Pde3b in the hypothalamus. Thus, to address the functional significance of hypothalamic phosphodiesterase-3B, we used Pde3b flox/flox and Nkx2.1-Cre mice to generate Pde3b Nkx2.1KD mice that showed 50% reduction of phosphodiesterase-3B in the hypothalamus. To determine the effect of partial ablation of phosphodiesterase-3B in the hypothalamus on energy and glucose homeostasis, males and females were subjected to either a low- or high-fat diet for 19–21 weeks. Only female but not male Pde3b Nkx2.1KD mice on the low-fat diet showed increased body weight from 13 weeks onward with increased food intake, decreased fat pad weights and hypoleptinemia. Glucose tolerance was improved in high-fat diet-fed male Pde3b Nkx2.1KD mice in association with decreased phosphoenolpyruvate carboxykinase-1 and glucose-6-phosphatase mRNA levels in the liver. Also, insulin sensitivity was increased in male Pde3b Nkx2.1KD mice on the low-fat diet. Changes in body weight or in glucose homeostasis were not associated with any alteration in hypothalamic proopiomelanocortin, neuropepide Y and agouti-related peptide mRNA levels. These results suggest that partial loss of phosphodiesterase-3B in the hypothalamus produces a sex-specific response in body weight and glucose homeostasis, and support a role, at least in part, for hypothalamic phosphodiesterase-3B in regulation of energy and glucose homeostasis in mice.

scholarly journals Effects of SCFA on the DNA methylation pattern of adiponectin and resistin in high-fat-diet-induced obese male mice

2018 ◽  
Vol 120 (4) ◽  
pp. 385-392 ◽  
Author(s):  
Yuanyuan Lu ◽  
Chaonan Fan ◽  
Aimin Liang ◽  
Xiuqin Fan ◽  
Rui Wang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Dna Methyltransferase ◽  
Methylation Pattern ◽  
Control Group ◽  
Mrna Levels ◽  
Male Mice ◽  
High Fat ◽  
Low Fat Diet

AbstractSpecific adipokines, such as adiponectin and resistin, are secreted from adipose tissue and are associated with the development of obesity. Supplementation of dietary SCFA can prevent and reverse high-fat-diet (HFD)-induced obesity. However, it is not clear whether SCFA ameliorate abnormal expression of adiponectin and resistin in the obese state. The aim of this study was to investigate the effects of SCFA on adiponectin and resistin’s expressions in diet-induced obese mice, as well as the potential mechanisms associated with DNA methylation. C57BL/6J male mice were fed for 16 weeks with five types of HFD (34·9 % fat by wt., 60 % kJ) – a control HFD and four HFD with acetate (HFD-A), propionate (HFD-P), butyrate (HFD-B) and their admixture (HFD-SCFA). Meanwhile, a low-fat diet (4·3 % fat by wt., 10 % kJ) was used as the control group. The reduced mRNA levels of adiponectin and resistin in the adipose tissue of the HFD-fed mice were significantly reversed by dietary supplementation of acetate, propionate, butyrate or their admixture to the HFD. Moreover, the expressional changes of adiponectin and resistin induced by SCFA were associated with alterations in DNA methylation at their promoters, which was mediated by reducing the expressions of enzyme-catalysed DNA methyltransferase (DNMT1, 3a, 3b) and the methyl-CpG-binding domain protein 2 (MBD2) and suppressing the binding of these enzymes to the promoters of adiponectin and resistin. Our results indicate that SCFA may correct aberrant expressions of adiponectin and resistin in obesity by epigenetic regulation.

scholarly journals AGE-RELATED MORPHO-FUNCTIONAL CHANGES IN RATS’ PANCREAS UNDER HIGH-FAT DIET-INDUCED INSULIN RESISTANCE AND ITS PHARMACOLOGICAL TREATMENT

2021 ◽  
Vol 74 (2) ◽  
pp. 241-246
Author(s):  
Tatiana Yu. Kvitnitskaya-Ryzhova ◽  
Halyna V. Kosiakova ◽  
Sergiy P. Lugovskoy ◽  
Sergiy A. Mykhalskiy ◽  
Pavlo P. Klymenko ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Age Groups ◽  
Protective Effects ◽  
High Fat ◽  
Compensatory Mechanisms ◽  
Important Indicator ◽  
Functional Changes ◽  
Insulin Resistant ◽  
Age Related ◽  
Pancreas Morphology

The aim: To determine the set of structural and functional changes in pancreatic islets (PI) of obesity-induced insulin resistant (IR) rats of different age (young and old) fed with prolonged (6 month) high-fat diet (HFD) (58% of fat) and further treatment with N-Stearoylethanolamine (NSE), a bioactive N-Acylethanolamine. Materials and methods: Alimentary obesity-induced IR model in rats of two age groups was used to investigate the influence of age and NSE treatment on pancreas morphology (using histological, histochemical and immunohistochemical techniques) and on several biochemical parameters associated with DM onset. Results: The NSE administration normalized pancreas morphology which was more affected in the old IR group; the signs of inflammation, edema, fibrosis and steatosis were somehow diminished and PI area became significantly increased. The amount of the A-F-positive insulocytes increased and TUNEL-positive – decreased. Compensatory hyperplasia in the affected pancreas of both age was an important indicator of NSE stimulating effect. Conclusions: Protective effects of NSE on morpho-functional state of pancreas in HFD-induced IR rats of both age are associated not only with its anti-inflammatory, anti-oxidant and anti-dyslipidemic properties but also with activation of PI hyperplasia and β-cells compensatory mechanisms.

scholarly journals Paternal Resistance Exercise Modulates Skeletal Muscle Remodeling Pathways in Fathers and Male Offspring Submitted to a High-Fat Diet

2021 ◽  
Vol 12 ◽  
Author(s):  
Rebecca Salomão ◽  
Ivo Vieira de Sousa Neto ◽  
Gracielle Vieira Ramos ◽  
Ramires Alsamir Tibana ◽  
João Quaglioti Durigan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Control Diet ◽  
Matrix Remodeling ◽  
Mrna Levels ◽  
High Fat ◽  
Protein Levels ◽  
Gene And Protein Expression ◽  
Muscle Homeostasis ◽  
Muscle Remodeling

Although some studies have shown that a high-fat diet (HFD) adversely affects muscle extracellular matrix remodeling, the mechanisms involved in muscle trophism, inflammation, and adipogenesis have not been fully investigated. Thus, we investigated the effects of 8 weeks of paternal resistance training (RT) on gene and protein expression/activity of critical factors involved in muscle inflammation and remodeling of fathers and offspring (offspring exposed to standard chow or HFD). Animals were randomly distributed to constitute sedentary fathers (SF; n = 7; did not perform RT) or trained fathers (TF n = 7; performed RT), with offspring from mating with sedentary females. After birth, 28 male pups were divided into four groups (n = 7 per group): offspring from sedentary father submitted either to control diet (SFO-C) or high-fat diet (SFO-HF) and offspring from trained father submitted to control diet (TFO-C) or high-fat diet (TFO-HF). Our results show that an HFD downregulated collagen mRNA levels and upregulated inflammatory and atrophy pathways and adipogenic transcription factor mRNA levels in offspring gastrocnemius muscle. In contrast, paternal RT increased MMP-2 activity and decreased IL-6 levels in offspring exposed to a control diet. Paternal RT upregulated P70s6k and Ppara mRNA levels and downregulated Atrogin1 mRNA levels, while decreasing NFκ-B, IL-1β, and IL-8 protein levels in offspring exposed to an HFD. Paternal physical training influences key skeletal muscle remodeling pathways and inflammatory profiles relevant for muscle homeostasis maintenance in offspring submitted to different diets.

scholarly journals Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Vol 21 (19) ◽  
pp. 7068
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
High Fat Diet ◽  
Intermittent Hypoxia ◽  
Environmental Changes ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder among the elderly, associated with aging and auditory hair cell death due to oxidative-stress-induced mitochondrial dysfunction. Although transgenic mice and long-term aging induction cultures have been used to study ARHL, there are currently no ARHL animal models that can be stimulated by intermittent environmental changes. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined on the basis of expression of hearing-loss-induced phenotypes and aging-related factors. The incidence of hearing loss was significantly higher in dual- and triple-exposure conditions than in intermittent hypoxic conditions, high-fat diet (HFD), or d-galactose injection alone. Continuous oxidative stress and HFD accelerated cellular aging. An increase in Ucp2, usually expressed during mitochondrial dysfunction, was observed. Expression of Cdh23, Slc26a4, Kcnq4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in the cells of the hearing organ. We found that intermittent hypoxia, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects the effects of intermittent environmental changes, will benefit future research on ARHL.

scholarly journals Estradiol Replacement Improves High-Fat Diet-Induced Obesity by Suppressing the Action of Ghrelin in Ovariectomized Rats

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 907
Author(s):  
Naoko Yokota-Nakagi ◽  
Haruka Takahashi ◽  
Mizuho Kawakami ◽  
Akira Takamata ◽  
Yuki Uchida ◽  
...  
Keyword(s):  
Growth Hormone ◽  
High Fat Diet ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
High Fat ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Protein Levels ◽  
Ovx Rats ◽  
Hypothalamic Arcuate Nucleus

This study aims to investigate the effects of estradiol replacement on the orexigenic action of ghrelin in ovariectomized (OVX) obese rats fed with a high-fat diet (HFD). Four weeks after OVX at 9 weeks of age, Wistar rats were subcutaneously implanted with either 17β-estradiol (E2) or placebo (Pla) pellets and started on HFD feeding. After 4 weeks, growth hormone-releasing peptide (GHRP)-6, a growth hormone secretagogue receptor (GHSR) agonist injected intraperitoneally, induced changes in HFD intake, and c-Fos-positive neurons in the hypothalamic arcuate nucleus (ARC) were measured in both groups. The ghrelin protein and mRNA levels, as well as GHSR protein in stomach, were analyzed by Western blotting and real-time PCR. HFD increased energy intake and body weight in the Pla group, while it temporarily reduced these in the E2 group. GHRP-6 enhanced HFD intake and activated neurons in the ARC only in the Pla group. Furthermore, gastric ghrelin and GHSR protein levels were lower in the E2 group than in the Pla group, but plasma acyl ghrelin levels were similar in both groups. Our results suggest that E2 replacement improves obesity by inhibiting the orexigenic action of ghrelin via downregulation of ghrelin and its receptor in stomach in HFD-fed OVX rats.

scholarly journals Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly. It is associated with aging and hair cell death due to oxidative stress-induced mitochondrial dysfunction. Although transgenic mice and long-term cultures for induction of aging have been used to study ARHL, there are presently no ARHL animal models stimulated by intermittent environmental change for aging. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined based on the expression of the hearing loss-induced phenotype and aging related factors in the short term. The incidence of hearing loss was significantly different among the groups subjected to intermittent hypoxic environment, high-fat diet (HFD), and injection with D-galactose. Continuous oxidative stress and HFD were factors that accelerated cellular aging. Increase in UCP2 affected oxidative stress and mitochondrial dysfunction. CDH23, SLC26A4, KCNQ4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in cells of the hearing organ. We found that intermittent hypoxic, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects intermittent environmental changes, will benefit future research on ARHL.

Sign in / Sign up

Export Citation Format

Share Document