Increased Lipid Accumulation in Liver and White Adipose Tissue in Aging in the SAMP10 Mouse

Honma, Tetsuo; Yanaka, Miyuki; Tsuduki, Tsuyoshi; Ikeda, Ikuo

doi:10.3177/jnsv.57.123

Cited by 33 publications

(35 citation statements)

References 39 publications

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“…3B and C). In addition, increased plasma insulin levels have also been observed in senescence-prone (SAMP10) mice and reported to explain the increased lipid accumulation with age in these mice [11]. However, since cytokines have been demonstrated to regulate CD36 expression at the transcriptional level [37], the possibility also arises that increased cytokine levels during hepatic inflammation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Sheedfar

Sung

Aparicio-Vergara

et al. 2014

Aging

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CD36 has been associated with obesity and diabetes in human liver diseases, however, its role in age-associated nonalcoholic fatty liver disease (NAFLD) is unknown. Therefore, liver biopsies were collected from individuals with histologically normal livers (n=30), and from patients diagnosed with simple steatosis (NAS; n=26). Patients were divided into two groups according to age and liver biopsy samples were immunostained for CD36. NAFLD parameters were examined in young (12-week) and middle-aged (52-week) C57BL/6J mice, some fed with chow-diet and some fed with low-fat (LFD; 10% kcal fat) or high-fat diet (HFD; 60% kcal fat) for 12-weeks. CD36 expression was positively associated with age in individuals with normal livers but not in NAS patients. However, CD36 was predominantly located at the plasma membrane of hepatocytes in aged NAS patients as compared to young. In chow-fed mice, aging, despite an increase in hepatic CD36 expression, was not associated with the development of NAFLD. However, middle-aged mice did exhibit the development of HFD-induced NAFLD, mediated by an increase of CD36 on the membrane. Enhanced CD36-mediated hepatic fat uptake may contribute to an accelerated progression of NAFLD in mice and humans. Therapies to prevent the increase in CD36 expression and/or CD36 from anchoring at the membrane may prevent the development of NAFLD.

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Section: Discussionmentioning

confidence: 99%

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Sheedfar

Sung

Aparicio-Vergara

et al. 2014

Aging

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“…But, to the extent of our current knowledge, no record on HFD-fed SAMP8 mice to study NAFLD is available. 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].…”

Section: Discussionmentioning

confidence: 99%

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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“…Thus, the SAMP10 mouse is widely used for analysis of mechanisms of aging (Shimada et al 2006;Unno et al 2007;Sasaki et al 2008;Tsuduki et al 2011;Honma et al 2011). In our previous study, we showed that SAMP10 mice fed a standard diet exhibited age-dependent increases of liver hydroxysteroid 11-beta dehydrogenase 1 (Hsd11b1) mRNA level, which promoted insulin secretion and insulin resistance and caused hyperinsulinemia and lipid accumulation in liver and white adipose tissue (Paterson et al 2004;Honma et al 2011). Hsd11b1 converts inert 11-dehydrocorticosterone into active corticosterone (Paterson et al 2004).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2011

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An understanding of the mechanisms of aging is important for prevention of age-related diseases. In this study, we examined age-dependent changes in lipid metabolism in the senescence-accelerated mouse (SAM)P10 fed a high-fat diet to investigate the effects of high-fat intake and aging. Tissue weights and biological parameters in plasma and liver were measured at 6 and 12 months old in SAMP10 mice fed a high-fat diet. These mice showed marked increases in liver triacylglycerol and plasma insulin levels with intake of a high-fat diet intake and aging. Lipid accumulation in hepatocytes and morphological aberrations and hypertrophy in pancreatic islets were also promoted by a high-fat diet and aging. To investigate the underlying mechanisms, the activities and mRNA levels for enzymes associated with lipid metabolism in liver were measured. The results indicated that the lipid metabolic system was activated by a high-fat diet and aging. Liver mRNA level for hydroxysteroid 11-beta dehydrogenase 1 (Hsd11b1), which exhibit age-dependent increases and promote insulin secretion, was also markedly increased. These results suggest that a high-fat diet accelerated aging in the liver of SAMP10 mice by increasing liver mRNA level for Hsd11b1, increasing insulin secretion, and promoting lipid accumulation in the liver.

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Increased Lipid Accumulation in Liver and White Adipose Tissue in Aging in the SAMP10 Mouse

Cited by 33 publications

References 39 publications

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

Increased hepatic CD36 expression with age is associated with enhanced susceptibility to nonalcoholic fatty liver disease

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

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

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