Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and epidemiologic studies have associated non-alcoholic fatty liver with the metabolic syndrome, with insulin resistance as the pivotal pathogenic factor. Obesity, type 2 diabetes mellitus, dyslipidemia, and hypertension contribute to risk for liver disease and to disease progression. The presence of multiple metabolic abnormalities is associated with the severity of liver disease. Patients have a high risk for cardiovascular morbidity and mortality, mediated by early atherosclerosis. This evidence has precise therapeutic implications: only a behavioral approach to lifestyle correction will address all alterations characterizing the metabolic syndrome, including metabolic liver disease.
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PMID:Metabolic syndrome and NASH. 1754 74

Non-alcoholic steatohepatitis (NASH) in obese and severely obese populations is associated with the metabolic syndrome, with features of the syndrome predicting those who will have NASH rather than simple steatosis, a more benign form of non-alcoholic fatty liver disease. Substantial weight loss is proving the most effective therapy for obesity-related conditions. Improvements have seen the development of less invasive procedures. There is growing evidence that laparoscopic adjustable gastric banding and roux-en-Y gastric bypass provide effective therapy.
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PMID:Surgical treatment for obesity and its impact on non-alcoholic steatohepatitis. 1754 76

Hepatocellular carcinoma (HCC) is part of the natural history of non-alcoholic steatohepatitis (NASH). A significant proportion of people who have cryptogenic cirrhosis develop HCC. NASH-related cirrhosis carries a substantial risk for early HCC development. Diagnosis of HCC often is made at first referral; the tumor usually is large with multiple localizations. Patients who have obesity or diabetes are at risk for HCC and a variety of cancers. Given the epidemic of obesity and diabetes, the incidence of NASH-related HCC is expected to increase. In addition to developing new diagnostic tools and pharmacologic therapies, efforts should be directed at preventing non-alcoholic fatty liver disease.
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PMID:Non-alcoholic steatohepatitis and cancer. 1754 79

Evidence-based management guidelines for non-alcoholic fatty liver disease (NAFLD) are lacking in the Asia-Pacific region or elsewhere. This review reports the results of a systematic literature search and expert opinions. The Asia-Pacific Working Party on NAFLD (APWP-NAFLD) has generated practical recommendations on management of NAFLD in this region. NAFLD should be suspected when there are metabolic risk factors and/or characteristic changes on hepatic ultrasonography. Diagnosis by ultrasonography, assessment of liver function and complications, exclusion of other liver diseases and screening for metabolic syndrome comprise initial assessment. Liver biopsy should be considered when there is diagnostic uncertainty, for patients at risk of advanced fibrosis, for those enrolled in clinical trials and at laparoscopy for another purpose. Lifestyle measures such as dietary restrictions and increased physical activity (aerobic exercise) should be encouraged, although the best management strategy to achieve this has yet to be defined. Complications of metabolic syndrome should be screened for regularly. Use of statins to treat hypercholesterolemia is safe and recommended; frequent alanine aminotransferase (ALT) monitoring is not required. Obese patients who do not respond to lifestyle measures should be referred to centers specializing in obesity management; consideration should be given to bariatric surgery or gastric ballooning. The role of pharmacotherapy remains investigational and is not recommended for routine clinical practice. Non-alcoholic fatty liver disease should be recognized as part of the metabolic syndrome and managed in a multidisciplinary approach that addresses liver disease in the context of risk factors for diabetes and premature cardiovascular disease. Lifestyle changes are the first line and mainstay of management.
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PMID:How should we manage patients with non-alcoholic fatty liver disease in 2007? 1756 32

In a population-based sample, after excluding alcohol consumption, hepatotoxic drugs and hepatitis B and C infected, we investigated if alanine-aminotransferase (ALT) was associated with metabolic syndrome and insulin resistance, and if this association was caused by non-alcoholic fatty liver disease (NAFLD). The sample (432 female and 119 male) was divided into two ALT thresholds corresponding to the 50th and 75th percentiles (P) (female > or = 15 and > or = 19 U/L; male > or = 17 and > or = 23 U/I, respectively). Blood pressure, body mass index, waist circumference, cholesterol, HDL cholesterol (HDLc), triglyceride (TG), TG/HDLc ratio, glycemia and homeostasis model assessment of insulin resistance (HOMA-IR) were compared between those above and below each ALT threshold. Female placed above the 50th P of ALT had higher levels of TG/HDLc ratio (p=0.029), glycemia (p=0.028), and homeostasis model assessment of insulin resistance, (p=0.045), and above the 75th P had higher SBP (p=0.036), DBP (p=0.018), TG (p=0.024), TG/HDLc ratio (p=0.028), glycemia (p=0.004) and HOMA-IR (p=0.0014). Male placed above the 50th P of ALT had higher BMI (p=0.017) and TG/HDLc ratio (p=0.048), and above the 75th P had lower values of HDLc (p=0.042). Only 16.5% of women and 14.5% of men, above the 75th P of ALT, showed an increase in liver brightness in the echography. This work shows in woman an early association of ALT with TG/HDLc ratio and HOMA-IR. Since the last two are independent predictors of cardiovascular risk, attention should be drawn to ALT values near the upper limit of the normal range even in the absence of NAFLD and obesity.
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PMID:Alanine-aminotransferase: an early marker for insulin resistance? 1759 95

Obesity is a chronic disease that has been considered an epidemic nowadays. It is associated to much co-morbidity, such as non-alcoholic fatty liver disease (NAFLD) and its complication, steatohepatitis. We report a case of a 58-year-old obese patient refractory to clinical treatment who was submitted to the use of intragastric balloon (BIB), developing steatohepatitis induced by fast weight loss.
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PMID:[Non-alcoholic steatohepatitis induced by fast weight loss during the use of intragastric balloon--a case report]. 1768 26

Non-alcoholic fatty liver disease is tightly associated with insulin resistance, type 2 diabetes and obesity, but the molecular links between hepatic fat accumulation and insulin resistance are not fully identified. Excessive accumulation of triglycerides (TG) is one the main characteristics of non-alcoholic fatty liver disease and fatty acids utilized for the synthesis of TG in liver are available from the plasma non-esterified fatty acid pool but also from fatty acids newly synthesized through hepatic de novo lipogenesis. Recently, the transcription factor ChREBP (carbohydrate responsive element binding protein) has emerged as a central determinant of lipid synthesis in liver through its transcriptional control of key genes of the lipogenic pathway, including fatty acid synthase and acetyl CoA carboxylase. In this mini-review, we will focus on the importance of ChREBP in the physiopathology of hepatic steatosis and insulin resistance by discussing the physiological and metabolic consequences of ChREBP knockdown in liver of ob/ob mice.
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PMID:Role of ChREBP in hepatic steatosis and insulin resistance. 1771 60

Fatty liver in obese patients is emerging as one of the most common causes of chronic liver disease. Obese patients are at risk of developing type 2 diabetes mellitus (DM), and aggravating non-alcoholic fatty liver disease (NAFLD), developing into steatohepatitis (NASH) and hepatic fibrosis. Little is known of the possible impact on liver fibrogenesis of diabetes type 2 associated with obesity and NAFLD. Fifty-two morbidly obese patients were evaluated with complete clinical and laboratory medical assessment. Liver biopsy material was fixed in formalin, routinely processed to paraffin blocks, cut into 4-microm sections, stained with HE, PAS, Masson's trichrome and reticulin. Immunohistochemical stains included collagen IV, SMA and laminin. Within the initial group of 52, 25 patients had DM type 2, mean age 45.8 years. Patients with diabetes were older; had higher BMI, liver enzyme tests, glucose, cholesterol, and triglycerides; and lower albumin concentration. Livers of diabetics had significantly more severe steatosis and rich perisinusoidal collagen IV, laminin and SMA accumulation without histologically detectable NASH and irrespective of the degree of steatosis. Obese patients with type 2 DM and insulin resistance develop more severe NAFLD and early sinusoidal fibrosclerosis.
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PMID:Fibrogenesis in fatty liver associated with obesity and diabetes mellitus type 2. 1784 88

Obesity induces an inflammation state that is implicated in many clinically important complications, including insulin resistance, diabetes, atherosclerosis and non-alcoholic fatty liver disease. Although the cause and the molecular participants in this process remain incompletely defined, adipose tissue has a central role. Obesity-induced production of pro-inflammatory molecules, typified by TNF-alpha was recognized more than a dozen years ago, and since then more than two dozen other pro-inflammatory molecules induced by obesity have been identified. More recently a critical role for immune cells, specifically mononuclear phagocytes, in generating the obesity-induced inflammation has been identified. Defining the molecular and cellular components of obesity-induced inflammation offers the potential of identifying therapeutic targets that can ameliorate the complications associated with obesity.
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PMID:Obesity-induced inflammation: a metabolic dialogue in the language of inflammation. 1787 76

Hepatocellular carcinoma (HCC) is increasing in frequency the USA. Age-adjusted incidence, hospitalization, and mortality rates have doubled over the past two decades. There are striking differences in the incidence of HCC related to age, gender, race, and geographic region. Although it remains an affliction of the elderly (mean age 65), there has been a considerable shift toward younger cases. There is a birth cohort effect with those born after 1945. Men are affected three times more frequently than women, Asians two times more than African American and Hispanic people, who are affected two times more often than Caucasians. However, the recent increase has disproportionately affected Caucasian (and Hispanic) men between ages 45 and 65. Hepatitis C virus (HCV) infection acquired 2-4 decades ago explains at least half of the observed increase in HCC; HCV-related HCC is likely tocontinue to increase for the next decade. A variable but significant proportion of cases (15-50%) do not have evidence for the risk factors of either viral hepatitis or heavy alcohol consumption. Insulin resistance syndrome manifesting as obesity and diabetes is emerging as a risk factor for HCC in the USA and may operate through the formation of non-alcoholic fatty liver disease (NAFLD); however, its effect on the current trend in HCC remains unclear. While there has been a small recent improvement in survival, it remains generally dismal (median 8 months). Population-based data in the USA indicate low application rate of HCC potentially curative therapy and marked regional differences.
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PMID:Epidemiology of hepatocellular carcinoma in USA. 1787 2


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