Sexual dimorphism in lipid metabolic phenotype associated with old age in Sprague–Dawley rats

Sanguino, Elena; Bejarano, R; Alegret, Marta; Sánchez, Rosa María Galán; Vázquez‐Carrera, Manuel; Laguna, Juan C.

doi:10.1016/j.exger.2004.06.007

Cited by 19 publications

(18 citation statements)

References 35 publications

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“…This suggests that the increase in the size and number of lipid droplets in HSC is related at least in part to an increase in retinoids in HSC. However, droplets also contain a similar amount of triglycerides, and there are reports of increased triglyceride content of old livers [17], but whether there is accumulation of triglycerides in HSC is not known.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Old Age on Hepatic Stellate Cells

Warren

Cogger

Fraser

et al. 2011

Current Gerontology and Geriatrics Research

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Aging is associated with marked changes in the hepatic sinusoid, yet the effect of old age on hepatic stellate cells (HSC) has not been well described. Transmission electron microscopy and immunohistochemistry were used to study the effects of aging on HSC in livers from rats (3-4 mths versus 24–27 mths) and mice (2-3 mths versus 20–22 mths). Desmin-positive HSC doubled in old age in both mice and rats. Alpha-smooth muscle actin- (αSMA-) positive cells did not increase significantly and remained only a small percentage of desmin-positive cells. Electron microscopy revealed that old age is associated with HSC that have a substantial increase in the number of lipid droplets which are larger in diameter. There was also a marked increase of HSC that protruded into the sinusoidal lumen in old mice. In conclusion, old age is associated with hyperplasia of HSC that are not activated and are engorged with lipid droplets.

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Section: Discussionmentioning

confidence: 99%

The Effects of Old Age on Hepatic Stellate Cells

Warren

Cogger

Fraser

et al. 2011

Current Gerontology and Geriatrics Research

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“…In addition, this lower downregulation of lipogenesis may explain the higher levels of triglycerides found in the liver of HF diet fed male rats. Males seem to be more prone to accumulating lipids in the liver because in other situations, such as ageing, old male rats present with a higher content of lipids in the liver than old female rats (27). Since fatty acid oxidation in the liver is regulated by PPAR‐α (28), the higher expression levels of this receptor found in male rats under the HF diet may serve to compensate for the lipid excess, by stimulating its β‐oxidation, as corroborated by the upregulation of CPT1L.…”

Section: Discussionmentioning

confidence: 99%

Sex‐differential Expression of Metabolism‐related Genes in Response to a High‐fat Diet

Priego

Sánchez

Picó

2008

Obesity

101

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objective: The aim of this work was to determine the sex-associated differences in the expression of genes related to lipid metabolism and fuel partitioning in response to a high-fat (HF) diet in rats, and whether this is linked to the higher tendency of males to suffer from metabolic disorders. Methods and Procedures: Male and female Wistar rats were fed for 6 months on a normal-fat (NF) or an HF diet. Body weight, fat depot weight, lipid concentration in liver, blood metabolites, and the expression of genes involved in fuel metabolism and partitioning in the liver, white adipose tissue (WAT), and skeletal muscle were measured. Results: Female rats fed on an HF diet gained more weight and had a greater increase in the adiposity index than male rats, while the circulating insulin levels remained unaltered; these animals also showed an increased expression of genes related to the energy influx in WAT and with fat utilization in skeletal muscle. Male but not female rats showed increased hepatic peroxisome proliferator-activated receptor-α (PPAR-α) and CPT1L mRNA expression, suggesting enhanced lipid handling and oxidation by this organ, and have a higher triacylglycerol content in liver. Male rats under the HF diet also displayed higher blood insulin levels. Discussion: These results show sex-dependent differences in lipid handling and partitioning between tissues in response to an HF diet, with females showing a higher capacity for storing fat in adipose tissue and for oxidizing fatty acids in muscle. These adaptations can help to explain the lower tendency of females to suffer from obesity-linked disorders under the conditions of an HF diet.

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“…These mechanisms may include enhanced fat uptake, increased de novo lipogenesis, decreased β‐oxidation, and/or decreased synthesis/secretion of very low‐density lipoproteins (Cohen et al ., ). Consistent with this, β‐oxidation has been reported to decline in livers with old age, involving reduced hepatic expression of nuclear receptor peroxisome proliferator‐activated receptor (Sanguino et al ., ). Other studies have highlighted an important role for augmented hepatic‐adrenergic signaling in the induction of liver steatosis with aging (Katz et al ., ; Ghosh et al ., ), although the specific mechanisms underlying β‐adrenergic‐mediated lipid accumulation with age remain undefined (Ghosh et al ., ).…”

Section: Aging and Nonalcoholic Fatty Liver Disease (Nafld)mentioning

confidence: 97%

Liver diseases and aging: friends or foes?

et al. 2013

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SummaryThe liver is the only internal human organ capable of natural regeneration of lost tissue, as little as 25% of a liver can regenerate into a whole liver. The process of aging predisposes to hepatic functional and structural impairment and metabolic risk. Therefore, understanding how aging could affect the molecular pathology of liver diseases is particularly important, and few studies to date have tackled this complex process. The most common liver disease, affecting one-third of the overall population, is nonalcoholic fatty liver disease (NAFLD), characterized by an intrahepatic accumulation of lipids. NAFLD can evolve into nonalcoholic steatohepatitis (NASH) in the presence of oxidative stress and inflammation. NASH is a serious risk factor for disabling and deadly liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). Old age seems to favor NAFLD, NASH, and ultimately HCC, in agreement with the inflamm-aging theory, according to which aging accrues inflammation. However, the incidence of HCC drops significantly in the very elderly (individuals aged more than 70) and the relationship between the progression of NAFLD/NASH/HCC and very old age is obscure. In this review, we discuss the literature and we argue that there might be an age window in which the liver becomes resistant to the development of injury; this needs to be studied to understand fully the interaction between age and liver diseases from a therapeutic perspective.

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Sexual dimorphism in lipid metabolic phenotype associated with old age in Sprague–Dawley rats

Cited by 19 publications

References 35 publications

The Effects of Old Age on Hepatic Stellate Cells

The Effects of Old Age on Hepatic Stellate Cells

Sex‐differential Expression of Metabolism‐related Genes in Response to a High‐fat Diet

Liver diseases and aging: friends or foes?

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