High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse

Honma, Tetsuo; Shinohara, Nahoko; Ito, Junya; Kijima, Ryo; Sugawara, Soko; Arai, Tatsuya; Tsuduki, Tsuyoshi; Ikeda, Ikuo

doi:10.1007/s10522-011-9363-2

Cited by 41 publications

(36 citation statements)

References 36 publications

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“…However, two recent studies compared HFD intake with standard chow feeding on hepatic changes in SAMP10) [23,24]. Their results showed that high-fat diet promoted lipid droplets accumulation in the livers of SAMP10 mice, contrary to normal chow feeding [23]. The same observation was confirmed by histopathological analysis of liver sections from SAMP8 mice groups in our model (Fig.…”

Section: Discussionsupporting

confidence: 78%

Bioactive Peptide Improves Diet-Induced Hepatic Fat Deposition and Hepatocyte Proinflammatory Response in SAMP8 Ageing Mice

DUmeUS¹,

Shibu²,

Lin³

et al. 2018

Cell Physiol Biochem

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Background/Aims: High-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) poses therapeutic challenges in elderly subjects. Due to lack of efficient drug therapy, plant-based bioactive peptides have been studied as alternative strategy in NAFLD and for less toxicity in elderly. To mimic fatty liver in aging conditions, researchers highly commended the genetically engineered strains SAMP8 (senescence-accelerated mice prone 8). However, there is a paucity of reports about the anti-steatosis effects of bioactive peptides against fatty liver development under a combined action of high-fat diet exposure and aging process. This study was conducted to evaluate the activity of DIKTNKPVIF peptide synthesized from alcalase-generated potato protein hydrolysate (PH), on reducing HFD-driven and steatosis-associated proinflammatory reaction in ageing model. Methods: Five groups of six-month-old SAMP8 mice (n=4, each) were fed either a normal chow (NC group) for 14 weeks upon sacrifice, or induced with a 6-week HFD feeding, then treated without (HCO group) or with an 8-week simultaneous administration of peptide (HPEP group), protein (HPH group) or probucol (HRX group). Liver organs were harvested from each group for histological analysis and immunoblot assay. Results: In contrast to NC, extensive fat accumulation was visualized in the liver slides of HCO. Following the trends of orally administered PH, intraperitoneally injected peptide reduces hepatic fat deposition and causes at protein level, a significant decrease in HFD-induced proinflammatory mediators p-p38 MAPK, FGF-2, TNF-α, IL-6 with concomitant reactivation of AMPK. However, p-Foxo1 and PPAR-α levels were slightly changed. Conclusion: Oral supplementation of PH and intraperitoneal injection of derived bioactive peptide alleviate proinflammatory reaction associated with hepatosteatosis development in elderly subjects, through activation of AMPK.

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Section: Discussionsupporting

confidence: 78%

Bioactive Peptide Improves Diet-Induced Hepatic Fat Deposition and Hepatocyte Proinflammatory Response in SAMP8 Ageing Mice

DUmeUS¹,

Shibu²,

Lin³

et al. 2018

Cell Physiol Biochem

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“…The interesting observation that may strengthen the close mechanistic relationship between aging and lipid overload are that caloric restriction potentially promotes longevity in many mammalian models, 47 whereas high-fat and/or -carbohydrate diets accelerates aging. 48 Furthermore, ischemic injury in the elderly and patients with hyperlipidemia is a major risk factor for ESRD. 49,50 In this point, therapeutic effort to restore lysosomal function and autophagic flux will pave the way to improving the clinical outcome of kidney injury related to aging or HFD.…”

Section: Discussionmentioning

confidence: 99%

High-Fat Diet–Induced Lysosomal Dysfunction and Impaired Autophagic Flux Contribute to Lipotoxicity in the Kidney

Yamamoto¹,

Takabatake²,

Takahashi³

et al. 2016

JASN

198

194

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Excessive fat intake contributes to the progression of metabolic diseases via cellular injury and inflammation, a process termed lipotoxicity. Here, we investigated the role of lysosomal dysfunction and impaired autophagic flux in the pathogenesis of lipotoxicity in the kidney. In mice, a high-fat diet (HFD) resulted in an accumulation of phospholipids in enlarged lysosomes within kidney proximal tubular cells (PTCs). In isolated PTCs treated with palmitic acid, autophagic degradation activity progressively stagnated in association with impaired lysosomal acidification and excessive lipid accumulation. Pulse-chase experiments revealed that the accumulated lipids originated from cellular membranes. In mice with induced PTC-specific ablation of autophagy, PTCs of HFD-mice exhibited greater accumulation of ubiquitin-positive protein aggregates normally removed by autophagy than did PTCs of mice fed a normal diet. Furthermore, HFD-mice had no capacity to augment autophagic activity upon another pathologic stress. Autophagy ablation also exaggerated HFD-induced mitochondrial dysfunction and inflammasome activation. Moreover, renal ischemia-reperfusion induced greater injury in HFD-mice than in mice fed a normal diet, and ablation of autophagy further exacerbated this effect. Finally, we detected similarly enhanced phospholipid accumulation in enlarged lysosomes and impaired autophagic flux in the kidneys of obese patients compared with nonobese patients. These findings provide key insights regarding the pathophysiology of lipotoxicity in the kidney and clues to a novel treatment for obesity-related kidney diseases.

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“…Reports show that health benefits of calorie restriction are mediated through the activation of sirtuins. The role of sirtuin is much relevant as HFD is known to accelerate aging and cause metabolic syndromes (Honma et al, 2012). Moreover, sirtuins are known to be effective regulators of Akt signalling and SIRT1 directly deacetylates Akt and promotes its activation (Pillai, Sundaresan, & Gupta, 2014).…”

Section: Fig 4 -Dapi and Tunel Staining To Detect Apoptosis Dapi Anmentioning

confidence: 99%

Potato protein hydrolysate attenuates high fat diet-induced cardiac apoptosis through SIRT1/ PGC-1á/Akt signalling

Huang

Chiang

Pai

et al. 2015

Journal of Functional Foods

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Available online A B S T R A C THigh-fat-diet (HFD)-induced obesity is a major contributor to diabetes and cardiovascular disease. In this research 6 week old male hamsters (n = 10) fed with HFD showed significant deterioration in heart function as determined from their cardiac ejection fraction percentage (EF%) and fraction shortening percentage (FS%). The number of apoptosis positive cells and the expression of protein markers of apoptosis drastically increased in the HFD-fed hamsters. However, the effects were significantly reduced following the administration of a lipolysis-stimulating peptide-APPH which was derived from the Alcalasehydrolysis of potato protein. Fifty days of APPH-treatment was effective in all the concentrations (15, 45 and 75 mg/kg/day) tested. The EF% and FS% measurements in the APPH treatment groups were comparable with that of the control group hamsters. The molecular events associated with the ameliorative effect of APPH were found to be potentially mediated by SIRT1 pathway indicating a restoration from the metabolic disorders induced by HFD.

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High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse

Cited by 41 publications

References 36 publications

Bioactive Peptide Improves Diet-Induced Hepatic Fat Deposition and Hepatocyte Proinflammatory Response in SAMP8 Ageing Mice

Bioactive Peptide Improves Diet-Induced Hepatic Fat Deposition and Hepatocyte Proinflammatory Response in SAMP8 Ageing Mice

High-Fat Diet–Induced Lysosomal Dysfunction and Impaired Autophagic Flux Contribute to Lipotoxicity in the Kidney

Potato protein hydrolysate attenuates high fat diet-induced cardiac apoptosis through SIRT1/ PGC-1á/Akt signalling

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