scholarly journals Conditional Loss of Ikkα in Sp7/osterix+ Cells Has No Effect on Bone, but Leads to Cell Autonomous, Age-related Loss of Peripheral Fat

2021 ◽  
Author(s):  
Jennifer L Davis ◽  
Nitin K Pokhrel ◽  
Linda Cox ◽  
Roberta Faccio ◽  
Deborah J Veis
Keyword(s):  
High Fat Diet ◽  
Fat Metabolism ◽  
Conditional Knockout ◽  
High Fat ◽  
Age Related ◽  
Reporter Mice ◽  
Upstream Kinase ◽  
Low Levels ◽  
Osteolineage Cells ◽  
Fat Pads

Abstract NF-κB has been reported to both promote and inhibit bone formation. To further explore its role in osteolineage cells, we conditionally deleted IKKα, an upstream kinase required for non-canonical NF-κB activation, using Sp7/Osterix (Osx)-Cre. Surprisingly, we found no effect on either cancellous or cortical bone, even following mechanical loading. However, we noted that IKKα conditional knockout (cKO) mice began to lose body weight after 6 months of age with severe reductions in fat mass in geriatric animals. Low levels of recombination at the IKKα locus were detected in fat pads isolated from 15 month old cKO mice. To determine if these effects were mediated by unexpected deletion of IKKα in peripheral adipocytes, we looked for Osx-Cre-mediated recombination in fat using reporter mice, which showed increasing degrees of reporter activation in adipocytes with age up to 18 months. Since Osx-Cre-driven recombination in peripheral adipocytes increases over time, we conclude that loss of fat in aged cKO mice is most likely caused by progressive deficits of IKKα in adipocytes. To further explore the effect of IKKα loss on fat metabolism, we challenged mice with a high fat diet at 2 months of age, finding that cKO mice gained less weight and showed improved glucose metabolism, compared to littermate controls. Thus, Osx-Cre mediated recombination beyond bone, including within adipocytes, should be considered as a possible explanation for extraskeletal phenotypes, especially in aging and metabolic studies.

scholarly journals The influence of dietary fat on fat metabolism and body Fat deposition in meal-feeding and nibbling rats

1975 ◽  
Vol 34 (1) ◽  
pp. 15-24 ◽  
Author(s):  
J. D. Wood ◽  
J. T. Reid
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Body Fat ◽  
High Fat Diet ◽  
Fat Metabolism ◽  
Dietary Fatty Acids ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Fat Pads

1. An experiment was done with rats (body-weight 160 g) to study the effects on fat metabolism and body composition of low (10 g/kg)- or high (140 g/kg)-fat diets fed as one meal for one 4 h period/d (meal-feeders) or as six spaced meals/d (nibblers). The daily energy intake/unit metabolic body-weight (body-weight0.73) was the same for all four groups, and this level of intake was about 80% of that consumed by rats allowed unrestricted access to the low-fat diet. The experimental period was 76 d.2. Rats given the high-fat diet deposited more body fat/d and, as a result, grew faster and were energetically more efficient than rats given the low-fat diet. The high-fat diet depressed de novo lipogenesis from glucose in epididymal and perirenal fat pads, whose fatty acid composition resembled that of the diet.3. For both diets meal-feeders had greater stomach plus small intestine weights than nibblers and had higher plasma free fatty acid levels, when they were killed 15 h after their last meal.4. Meal-feeders given the low-fat diet had the greatest rate of lipogenesis for fat pads.5. Meal-feeders given the high-fat diet deposited less of the main dietary fatty acids in their fat pads.6. There was no evidence that meal-feeders eating a high-fat diet adapt their metabolism so completely that they become more efficient utilizers than those nibbling this diet. Meal-feeders eating the low-fat diet became no fatter than nibblers of this diet, possibly because they were eating less than their daily ad lib. intake.

Hyperbaric oxygen therapy attenuates D-galactose-induced-age-related cardiac dysfunction through mitigating cardiac mitochondrial dysfunction in pre-diabetic rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Bo-Htay ◽  
T Shwe ◽  
S Palee ◽  
T Pattarasakulchai ◽  
K Shinlapawittayatorn ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
Normal Diet ◽  
Lv Function ◽  
High Fat ◽  
Insulin Resistant ◽  
Lv Dysfunction ◽  
Age Related ◽  
Mitochondrial Functions

Abstract Background D-galactose (D-gal) induced ageing has been shown to exacerbate left ventricular (LV) dysfunction via worsening of apoptosis and mitochondrial dysfunction in the heart of obese rats. Hyperbaric oxygen therapy (HBOT) has been demonstrated to exert anti-inflammatory and anti-apoptotic effects in multiple neurological disorders. However, the cardioprotective effect of HBOT on inflammation, apoptosis, LV and mitochondrial functions in D-gal induced ageing rats in the presence of obese-insulin resistant condition has never been investigated. Purpose We sought to determine the effect of HBOT on inflammation, apoptosis, mitochondrial functions and LV function in pre-diabetic rats with D-gal induced ageing. We hypothesized that HBOT attenuates D-gal induced cardiac mitochondrial dysfunctions and reduces inflammation and apoptosis, leading to improved LV function in pre-diabetic rats. Methods Forty-eight male Wistar rats were fed with either normal diet or high-fat diet for 12 weeks. Then, rats were treated with either vehicle groups (0.9% NSS, subcutaneous injection (SC)) or D-gal groups (150 mg/kg/day, SC) for 8 weeks. At week 21, rats in each group were equally divided into 6 sub-groups: normal diet fed rats treated with vehicle (NDV) sham, normal diet fed rats treated with D-gal (NDDg) sham, high fat diet fed rats treated with D-gal (HFDg) sham, high fat diet fed rats treated with vehicle (HFV) + HBOT, NDDg + HBOT and HFDg + HBOT. Sham treated rats were given normal concentration of O2 (flow rate of 80 L/min, 1 ATA for 60 minutes), whereas HBOT treated rats were subjected to 100% O2 (flow rate of 250 L/min, 2 ATA for 60 minutes), given once daily for 2 weeks. Results Under obese-insulin resistant condition, D-gal-induced ageing aggravated LV dysfunction (Fig 1A) and impaired cardiac mitochondrial function, increased cardiac inflammatory and apoptotic markers (Fig 1B). HBOT markedly reduced cardiac TNF-α level and TUNEL positive apoptotic cells, and improved cardiac mitochondrial function as indicated by decreased mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, resulting in the restoration of the normal LV function in HFV and NDDg rats, compared to sham NDDg rats. In addition, in HFDg treated rats, HBOT attenuated cardiac TNF-α level, TUNEL positive apoptotic cells and cardiac mitochondrial dysfunction, compared to sham HFDg rats, leading to improved cardiac function as indicated by increased %LV ejection fraction (LVEF) (Figure 1). Conclusion HBOT efficiently alleviates D-gal-induced-age-related LV dysfunction through mitigating inflammation, apoptosis and mitochondrial dysfunction in pre-diabetic rats. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): 1. The National Science and Technology Development Agency Thailand, 2. Thailand Research Fund Grants

scholarly journals Tissue-specific expression of Sprouty1 in mice protects against high-fat diet-induced fat accumulation, bone loss and metabolic dysfunction

2011 ◽  
Vol 108 (6) ◽  
pp. 1025-1033 ◽  
Author(s):  
Sumithra Urs ◽  
Terry Henderson ◽  
Phuong Le ◽  
Clifford J. Rosen ◽  
Lucy Liaw
Keyword(s):  
Adipose Tissue ◽  
Bone Loss ◽  
Bone Mass ◽  
Body Fat ◽  
High Fat Diet ◽  
Conditional Knockout ◽  
Whole Body ◽  
High Fat ◽  
Tissue Specific ◽  
Diet Induced Obesity

We recently characterised Sprouty1 (Spry1), a growth factor signalling inhibitor as a regulator of marrow progenitor cells promoting osteoblast differentiation at the expense of adipocytes. Adipose tissue-specific Spry1 expression in mice resulted in increased bone mass and reduced body fat, while conditional knockout of Spry1 had the opposite effect with decreased bone mass and increased body fat. Because Spry1 suppresses normal fat development, we tested the hypothesis that Spry1 expression prevents high-fat diet-induced obesity, bone loss and associated lipid abnormalities, and demonstrate that Spry1 has a long-term protective effect on mice fed a high-energy diet. We studied diet-induced obesity in mice with fatty acid binding promoter-driven expression or conditional knockout of Spry1 in adipocytes. Phenotyping was performed by whole-body dual-energy X-ray absorptiometry, microCT, histology and blood analysis. In conditional Spry1-null mice, a high-fat diet increased body fat by 40 %, impaired glucose regulation and led to liver steatosis. However, overexpression of Spry1 led to 35 % (P < 0·05) lower body fat, reduced bone loss and normal metabolic function compared with single transgenics. This protective phenotype was associated with decreased circulating insulin (70 %) and leptin (54 %; P < 0·005) compared with controls on a high-fat diet. Additionally, Spry1 expression decreased adipose tissue inflammation by 45 %. We show that conditional Spry1 expression in adipose tissue protects against high-fat diet-induced obesity and associated bone loss.

scholarly journals Curcumin Inhibits Age-Related Vascular Changes in Aged Mice Fed a High-Fat Diet

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1476 ◽  
Author(s):  
Kenichiro Takano ◽  
Junko Tatebe ◽  
Naohiro Washizawa ◽  
Toshisuke Morita
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Heme Oxygenase 1 ◽  
Vascular Aging ◽  
High Fat ◽  
Sirt1 Expression ◽  
Age Related ◽  
Westernized Diet ◽  
Term Administration ◽  
Oxidative Effects

Inhibiting the onset of arteriosclerotic disease, which has been increasing due to the westernized diet and aging, is a significant social challenge. Curcumin, a type of polyphenol, has anti-oxidative effects and anti-inflammatory action and is expected to treat and to have prophylactic effects on different diseases. In this study, we examined the effects of long-term administration of curcumin on vascular aging and chronic inflammation—the causes of arteriosclerotic disease. Eight-week-old C57BL/6J mice were fed with high fat diet (HFD) or 0.1% curcumin-mixed HFD (HFD + Cu) until 80 weeks old (n = 20 for each group). After the breeding, we examined the expression of antioxidant enzymes, heme oxygenase-1 (HO-1), oxidative stress, vascular aging, and inflammatory changes in the aorta. In the HFD group, oxidative stress increased with decreased sirt1 expression in the aorta followed by increased senescent cells and enhanced inflammation. Whereas in the HFD + Cu group, HO-1 was induced in the aorta with the suppression of oxidative stress. Additionally, it was shown that sirt1 expression in the aorta in the HFD + Cu group remained at a level comparable to that of the 8-week-old mice with suppression of increased senescent cells and enhanced inflammation. Consequently, disorders associated with HFD were resolved. These results suggest that curcumin might be a food with a prophylactic function against arteriosclerotic disease.

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-&beta;, Il-6, Tnf-&alpha;, Cxcl-10, Mcp-1 and Tgf-&beta;1 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 High-fat diet increases NF-κB signaling in the prostate of reporter mice

The Prostate ◽  
2010 ◽  
Vol 71 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Eugene V. Vykhovanets ◽  
Eswar Shankar ◽  
Olena V. Vykhovanets ◽  
Sanjeev Shukla ◽  
Sanjay Gupta
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Reporter Mice

Abstract 15294: Activation of Mac-1 Integrin Prevents G-CSF Mediated Monocyte Mobilization and Atherosclerosis Severity in Hypercholesterolemic Mice

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sina Rahimpour ◽  
Annia Mesa ◽  
Lei Song ◽  
Natasha Fernandez ◽  
Si M Pham ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Plasma Lipid ◽  
High Fat ◽  
Once Daily ◽  
Leukocyte Mobilization ◽  
Sudan Iv ◽  
Low Levels ◽  
Atherosclerosis Development ◽  
Excessive Number ◽  
Atherosclerosis Severity

Background: Leukadherins (LA) are a novel family of Mac-1 agonists that increase cell adhesion and prevent leukocyte mobilization and tissue inflammation. This study brings new insights into how leukadherin LA1 protects hypercholesterolemic ApoE-null mice from excessive atherosclerosis development. Hypothesis: Activation of Mac-1 integrin with leukadherin LA1 retains monocytes in medullary and extramedullary centers and therefore, controls high fat diet induced monocytosis and atherosclerosis in ApoE-null mice. Methods and Results: Once daily administration of LA1 (10mg/kg) for 16 weeks significantly reduced atherosclerosis in the entire aorta and the aortic valve of high fat diet fed ApoE-null mice as determined by Sudan IV staining. The LA1 treatment had not effect on body weight or plasma lipid levels though it significantly reduced the number of circulating monocytes (Lin2- CD11c- CD11b+ by FACS). The remaining circulating monocytes in LA1-treated mice displayed low levels of Ly6C, a marker for inflammation. Interestingly, LA1 caused monocyte retention in the bone marrow (BM) and macrophages (F4/80+ by IHC) in the spleen of hypercholesterolemic mice, which account for the low numbers of monocytes seem in the circulation of these mice. On the other hand, the excessive number of BM monocytes didn’t compromise the number of hematopoietic (Lin- Sca+ c-Kit+) or myeloid (Lin- Sca- c-Kit+) progenitor cells. Finally, we assessed the effect of LA1 on systemic inflammatory mediators using multiplex immunoassay. The plasma levels of G-CSF, one of the main monocyte mobilization cytokines capable of promoting atherosclerosis in ApoE-null mice, were found reduced in a half in treated versus control mice. Conclusions: These data demonstrate that Mac-1 activation with LA1 significantly reduces atherosclerosis in hypercholesterolemic ApoE-null by impairing G-CSF mediated monocyte mobilization from medullary and extramedullary centers.

scholarly journals Benjankul supplementation improves hepatic fat metabolism in high-fat diet-induced obese rats

2020 ◽  
Vol 19 (4) ◽  
pp. 797-803
Author(s):  
Achiraya Kamchansuppasin ◽  
Kevalin Vongthoung ◽  
Pomthep Temrangsee ◽  
Narongsuk Munkong ◽  
Nusiri Lerdvuthisopon
Keyword(s):  
High Fat Diet ◽  
Fat Metabolism ◽  
High Fat ◽  
Obese Rats ◽  
Hepatic Fat

No Abstract.

scholarly journals Age-related change in anti-platelet aggregation in feeding of a high fat diet and ω-3 fatty acid in rats

1995 ◽  
Vol 67 ◽  
pp. 165
Author(s):  
Hossain Md Shahdat ◽  
Michio Hashimoto ◽  
Toshiko Hara ◽  
Suntio Masumura
Keyword(s):  
Fatty Acid ◽  
Platelet Aggregation ◽  
High Fat Diet ◽  
High Fat ◽  
Age Related

Lactobacilli modulated AMPK activity and prevented telomere shortening in ageing rats

2019 ◽  
Vol 10 (8) ◽  
pp. 883-892
Author(s):  
L.C. Lew ◽  
Y.Y. Hor ◽  
M.H. Jaafar ◽  
A.S.Y. Lau ◽  
J.S. Ong ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Rat Model ◽  
High Fat Diet ◽  
Lactobacillus Reuteri ◽  
Plasma Lipid ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
High Fat ◽  
Age Related ◽  
Plasma Lipid Peroxidation

This study aimed to evaluate the anti-ageing effects of different strains of lactobacilli putative probiotics on an ageing rat model as induced by D-galactose and a high fat diet. Male Sprague-Dawley rats were fed with high fat diet (54% kcal fat) and injected with D-galactose daily for 12 weeks to induce ageing. The effects of putative probiotic strains on age-related impairment such as telomere length, plasma lipid peroxidation, hepatic 5’adenosine monophosphate-activated protein kinase (AMPK) expression, as well as endurance performance were evaluated. Administration of statin, Lactobacillus plantarum DR7 (LP-DR7), Lactobacillus fermentum DR9 (LF-DR9), and Lactobacillus reuteri 8513d (LR-8513d) significantly reduced the shortening of telomere and increased the expression of AMPK subunit-α1 (P<0.05). Plasma lipid peroxidation was lower (P<0.05) in groups administered with statin and LF-DR9 as compared to the control. AMPK subunit-α2 was elevated in rats administered with LP-DR7 as compared to the control (P<0.05). Using an in vivo ageing rat model, the current study has illustrated the potentials of lactobacilli putative probiotics in alleviation of age-related impairment in a strain-dependent manner.

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