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Query: UMLS:C0015695 (fatty liver)
13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated plasma lipids, glucose, insulin, and fatty liver are among components of metabolic syndrome, a phenotypic pattern that typically precedes the development of Type 2 diabetes. Animal studies show that intake of anthocyanins reduces hyperlipidemia, obesity, and atherosclerosis and that anthocyanin-rich extracts may exert these effects in association with altered activity of tissue peroxisome proliferator-activated receptors (PPARs). However, studies are lacking to test this correlation using physiologically relevant, whole food sources of anthocyanins. Tart cherries are a rich source of anthocyanins, and whole cherry fruit intake may also affect hyperlipidemia and/or affect tissue PPARs. This hypothesis was tested in the Dahl Salt-Sensitive rat having insulin resistance and hyperlipidemia. For 90 days, Dahl rats were pair-fed AIN-76a-based diets supplemented with either 1% (wt:wt) freeze-dried whole tart cherry or with 0.85% additional carbohydrate to match macronutrient and calorie provision. After 90 days, the cherry-enriched diet was associated with reduced fasting blood glucose, hyperlipidemia, hyperinsulinemia, and reduced fatty liver. The cherry diet was also associated with significantly enhanced hepatic PPAR-alpha mRNA, enhanced hepatic PPAR-alpha target acyl-coenzyme A oxidase mRNA and activity, and increased plasma antioxidant capacity. In conclusion, physiologically relevant tart cherry consumption reduced several phenotypic risk factors that are associated with risk for metabolic syndrome and Type 2 diabetes. Tart cherries may represent a whole food research model of the health effects of anthocyanin-rich foods and may possess nutraceutical value against risk factors for metabolic syndrome and its clinical sequelae.
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PMID:Altered hyperlipidemia, hepatic steatosis, and hepatic peroxisome proliferator-activated receptors in rats with intake of tart cherry. 1859 66

Integration of metabolism and immunity in normal physiology is beneficial to maintain homeostasis. It can also become deleterious under conditions such as the immunosuppression observed among the malnourished. With the increase of excess weight and obesity, a new set of problems and complications has emerged at the intersection of metabolic activity and immunity. As examples of the latter we find obesity associated with inflammatory diseases, diabetes, fatty liver disease and atherosclerosis. Obesity is characterized by inflammation; there are common factors at the crossroads of inflammation and metabolic disease. Obesity is characterized by an inflammatory response and many inflammatory mediators exhibit expression patterns that interfere with insulin action. The high level of coordination of inflammatory and metabolic pathways is highlighted by the overlapping biology of macrophage and adipocite function observed in obesity. The intracellular signaling pathways activated by inflammatory and stress responses inhibit insulin signaling and the loss of inflammatory mediators prevents insulin resistance. In the absence of obesity, an infusion of inflammatory cytokines or lipids causes insulin resistance. Understanding the mechanisms leading from obesity to inflammation will have important implications to help reduce the morbidity and mortality associated with obesity by preventing its association with inflammatory disorders.
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PMID:[Obesity, inflammation and diabetes]. 1861 57

Emerging attention has been paid to metabolic syndrome, which comprises several metabolic disorders including visceral obesity, diabetes mellitus, dyslipidemia, and hypertension. Whether the severity of each disease is mild to moderate, the comorbidity of these metabolic disorders has a serious impact on the development of atherosclerosis. Nonalcoholic fatty liver disease (NAFLD) is the major hepatic disorder in patients with metabolic syndrome, and indeed it is the most common cause of abnormal liver function tests in the working population in industrialized countries. In recent years, it has become recognized that NAFLD is no longer just a trivial disease, and a rather considerable proportion of the patients develop liver cirrhosis. Furthermore, chronic infection of hepatitis C virus also develops a pathological feature of steatohepatitis, and extended hepatic steatosis has a serious impact not only on the progression of hepatic fibrosis but also on the antiviral efficacy of interferon therapy. Emerging lines of studies indicated that insulin resistance, abnormal lipid metabolism, and dysregulation of cytokines/adipokines (e.g., tumor necrosis factor-alpha, adiponectin, and leptin) are profoundly involved in the pathogenesis of NAFLD. This review aims to integrate the reported evidence and to provide the current point of view for comprehensive understanding of the pathophysiology of steatohepatitis.
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PMID:Liver diseases and metabolic syndrome. 1864 37

Obesity is an inflammatory disorder characterized by heightened activity of the innate immune system. Innate immune activation is central to the development of obesity-related insulin resistance; it also plays an important role in obesity-related tissue damage, such as that seen in atherosclerosis. Recent research has implicated the innate immune system in the pathophysiology of obesity-related liver disease. This review summarizes how innate immune processes, occurring both within and outside the liver, cause not only insulin resistance but also end-organ damage in the form of nonalcoholic fatty liver disease.
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PMID:Beyond insulin resistance: Innate immunity in nonalcoholic steatohepatitis. 1866 25

The ability to store energy in the form of energy-dense TAG (triacylglycerol) and to mobilize these stores rapidly during times of low carbohydrate availability (fasting or famine) or during heightened metabolic demand (exercise or cold-stress) is a highly conserved process essential for survival. Today, in the presence of nutrient excess and sedentary lifestyles, the regulation of this pathway is viewed as an important therapeutic target for disease prevention, as elevated circulating fatty acids in obesity contribute to many aspects of the metabolic syndrome including hepatic steatosis, atherosclerosis and insulin resistance. In the present review, we discuss the metabolic regulation and function of TAG lipases with a focus on HSL (hormone-sensitive lipase), ATGL (adipose triacylglycerol lipase) and newly identified members of the lipolytic proteome.
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PMID:Regulation and function of triacylglycerol lipases in cellular metabolism. 1871 47

An association between non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD) has been recently suggested. Indeed, different studies have demonstrated that NAFLD patients present increased subclinical atherosclerosis compared to non-steatosic individuals, and are supported by the few follow-up studies revealing that CVD is the second most common cause of death in NAFLD patients. However, the nature of the relationship NAFLD/CVD is still under debate: is NAFLD a consequence of, or a contributor to, the dysmetabolic cascade leading to atherosclerosis? In this issue of the journal, McKimmie and coauthors analyzed a subset of 623 participants from the Diabetes Heart Study for hepatic steatosis, classic CVD risk factors, subcutaneous and visceral fat, coronary, aortic and carotid artery calcium, and carotid intima-media thickness. After adjusting for all the CVD risk factors plus visceral fat, they did not find independent associations between steatosis and the cardiovascular markers of interest, and conclude that NAFLD may be best described as an epiphenomenon in this context. The strength of this study resides in the numerosity of the sample, the broad cardiovascular examination, and the direct assessment by computed tomography of visceral fat, an undisputed major contributor to NAFLD, the metabolic syndrome and atherosclerosis. However, waiting for prospective and interventional studies in order to definitely determine the nature of the relationship NAFLD/CVD, sufficient evidence exists to derive a first message and transfer it into the clinical practice: an overall assessment of the CVD risk, and the aggressive management of the atherosclerotic risk factors, seem mandatory in all NAFLD patients.
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PMID:Association between non-alcoholic fatty liver disease and cardiovascular disease: a first message should pass. 1885 70

In recent years, the association between hyperlipidemia and the development of arteriosclerosis has been addressed in several studies. Rabbit models of hypertriglyceridemia (TGH) and postprandial hypertriglyceridemia (PHT) have been developed at the authors' institute. TGH rabbits manifest pathology similar to that of humans with TGH, such as xanthoma, in addition to atherosclerosis of arterioles. Furthermore, PHT rabbits show visceral obesity, insulin resistance, and impaired glucose tolerance, with pathologic features similar to those of the metabolic syndrome assumed to be the cause of human ischemic heart disease. This study was designed to investigate the histopathologic features of TGH and PHT rabbits. TGH rabbits showed advanced aortic atherosclerosis, accompanied by intimal thickening of coronary and renal arteries, fatty liver changes, and xanthoma. PHT rabbits demonstrated aortic intimal thickening and hepatic fatty degeneration. The results of this study suggest that TGH and PHT rabbits are useful animal models for studying human hyperlipidemia and metabolic syndrome and the cardiovascular diseases that result from these conditions.
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PMID:Pathologic findings in rabbit models of hereditary hypertriglyceridemia and hereditary postprandial hypertriglyceridemia. 1900 73

Adipose tissue is critical in energy homeostasis. Adipose tissue 'buffers' the lipids and energy rich compounds which are pumped into the blood stream soon after meals. It senses, signals other organs like liver and brain about the energy reserves via adipokines. Adiponectin, the most abundant adipokine has insulin sensitizing, anti-inflammatory antiatherogenic and antisteatotic effects. Adipose tissue dysfunction is accompanied by abnormal lipid distribution and storage which contributes to diseases like diabetes, nonalcoholic fatty liver disease and atherosclerosis. Obesity and lipodystrophy are associated with dysfunctional adipocytes. Pre-adipocytes are easy to isolate and culture. A personalized depot specific liposuction to remove the inactive adipocytes followed by adipocyte repopulation could be useful in the treatment of these diseases.
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PMID:Adipose tissue transplantation may be a potential treatment for diabetes, atherosclerosis and nonalcoholic steatohepatitis. 1904 21

The storage of fatty acids and fatty alcohols in the form of neutral lipids such as triacylglycerol (TAG), cholesteryl ester (CE), and wax ester (WE) serves to provide reservoirs for membrane formation and maintenance, lipoprotein trafficking, lipid detoxification, evaporation barriers, and fuel in times of stress or nutrient deprivation. This ancient process likely originated in actinomycetes and has persisted in eukaryotes, albeit by different molecular mechanisms. A surfeit of neutral lipids is strongly, perhaps causally, related to several human diseases such as diabetes mellitus, obesity, atherosclerosis and nonalcoholic fatty liver disease. Therefore, understanding the metabolic pathways of neutral lipid synthesis and the roles of the enzymes involved may facilitate the development of new therapeutic interventions for these syndromes.
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PMID:The genetics of neutral lipid biosynthesis: an evolutionary perspective. 1911 72

Recent studies have suggested that milk and certain dairy food components have the potential to protect against cardiovascular disease. In order to determine whether the addition of milk-derived phospholipids to the diet results in an improvement in metabolic and cardiovascular risk factors, we studied four groups (n=10) of C57BL/6 mice that were fed: (1) a normal non-purified diet (N); (2) the normal non-purified diet supplemented with phospholipid-rich dairy milk extract (PLRDME, 2.5% by wt) (NPL); (3) a high-fat semi-purified diet (HF) containing 21% butterfat+0.15% cholesterol by wt; or (4) HF supplemented with 2.5% by wt PLRDME (HFPL). Dietary PLRDME supplementation did not have a significant effect on metabolic parameters in mice fed the N diet. In contrast, in high-fat fed mice, PLRDME caused a significant decrease in: (a) liver wt (1.57+/-0.06 g vs. 1.20+/-0.04 g, P<0.001), (b) total liver lipid (255+/-22 mg vs. 127+/-13 mg, P<0.001, (c) liver triglyceride (TG) and total cholesterol (TC) 236+/-25 micromol/g vs. 130+/-8 micromol/g (P<0.01), 40+/-7 micromol/g vs. 21+/-2 micromol/g (P<0.05), respectively); and serum lipids (TG: 1.4+/-0.1 mmol/L vs. 1.1+/-0.1 mmol/L, P=0.01; TC: 4.6+/-0.2 mmol/L vs. 3.6+/-0.2 mmol/L, P<0.001; and PL: 3.3+/-0.1 mmol/L vs. 2.6+/-0.1 mmol/L, P<0.01). These data indicate that dietary PLRDME has a beneficial effect on hepatomegaly, hepatic steatosis and elevated serum lipid levels in mice fed a high-fat diet, providing evidence that PLRDME might be of therapeutic value in human subjects as a hepatoprotective or cardioprotective nutraceutical.
Atherosclerosis 2009 Jul
PMID:Dietary phospholipid-rich dairy milk extract reduces hepatomegaly, hepatic steatosis and hyperlipidemia in mice fed a high-fat diet. 1915 82


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