Insulin resistance and metabolic syndrome in patients with NAFLD but without diabetes: Effect of a 6 month regime intervention

Department of Gastroenterology, Hacettepe University, Engüri, Ankara, Turkey
Acta gastro-enterologica Belgica (Impact Factor: 0.91). 07/2007; 70(3):253-9.
Source: PubMed


Non-alcoholic fatty liver disease (NAFLD) and the metabolic syndrome are two intertwined diseases sharing the same factor in their pathogenesis; insulin resistance. The aim of the study was to establish a link between glucose tolerance and NAFLD.
Fifty-two non-diabetic NAFLD patients were included in the study. Inclusion criteria were elevated alanine aminotransferase (ALT), hyperechogenic liver detected at ultrasonography, and exclusion of other causes of liver disease. Hepatobiliary ultrasonography and laboratory tests including biochemical and metabolic profiles were performed; HOMA insulin resistance was calculated.
The mean age was 43 years, and 61% were male. More than a two fold increase in alanine aminotransferase levels was seen in 37% of the patients. Serum levels of aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase (ALP) were elevated in 36%, 46%, and 30% of patients respectively. Low HDL-C levels were found in 46% and high LDL-C levels in 25%. Other results of note were elevated lipoprotein-a levels in 40%, impaired fasting glucose in 23%, impaired glucose tolerance in 26%, elevated fasting c-peptide levels in 61%, and elevated fasting serum insulin levels in 11% of patients. In 30% of patients, body mass index was over 30 kg/m2 and 78% had a waist-hip ratio more than 0.9. HOMA insulin resistance was significantly related with elevated ALP levels and hepatomegaly. Following a 6 months treatment with a standard diet, liver enzymes and metabolic parameters both improved. Only 7 patients had persistently high liver enzymes.
Basal insulin levels and the oral glucose tolerance test should be an integral part of the evaluation of patients with NAFLD. The association between NAFLD and metabolic syndrome as well as the benefits of dieting on preventing progression of NAFLD should be stressed.

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    • "NAFLD is a component of metabolic syndrome which comprises central obesity, hypertension, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), hypertriglyceridemia, and low HDL.[28] Metabolic syndrome is a risk factor for type II diabetes mellitus, coronary artery disease, and cerebro-vascular disease.[29] "
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    ABSTRACT: As a major organ of intermediary metabolism, the liver is exposed to a variety of metabolic insults due to diseases and xenobiotics viz., insulin resistance (IR) drugs, toxins, microbial products, etc. One of the consequences of these metabolic insults including obesity and type 2 diabetes mellitus is the development of non-alcoholic fatty liver disease (NAFLD). The recent alarming increase in the prevalence of NAFLD compels the need to develop an appropriate animal model of the disease so as to evolve effective interventions. In this study, we have developed, in the rat, a new model of NAFLD showing several key features akin to the disease in humans. Male Wistar rats were challenged with 30% high fat diet (HFD) – butter, for 2 weeks to induce NAFLD. A hydroalcoholic extract of Picrorhiza kurroa was administered to study the possible reversal of fatty changes in the liver. The extract was given in two doses viz., 200mg/kg and 400 mg/kg b.i.d., p.o. for a period of 4 weeks. There were three control groups (n = 6/group) – vehicle with a regular diet, vehicle with HFD, and HFD with silymarin – a known hepatoprotective. Histopathology showed that the P. kurroa extract brought about a reversal of the fatty infiltration of the liver (mg/g) and a lowering of the quantity of hepatic lipids (mg/g) compared to that in the HFD control group (38.33 ± 5.35 for 200mg/kg; 29.44 ± 8.49 for 400mg/kg of P. kurroa vs.130.07 ± 6.36mg/g of liver tissue in the HFD control group; P<0.001). Compared to the standard dose of the known hepatoprotective silymarin, P. kurroa reduced the lipid content (mg/g) of the liver more significantly at the dose of 400mg/kg (57.71 ± 12.45mg/kg vs. 29.44 ± 8.49 for the silymarin group vs. 400mg/kg of P. kurroa, P<0.001). In view of the increasing prevalence of metabolic syndrome and NAFLD, P. kurroa should be investigated by the reverse pharmacology path as a potential drug for the treatment of NAFLD, and essential safety studies and preformulation research for concentration of the putative actives should be carried out.
    No preview · Article · Jul 2010 · Journal of Ayurveda and integrative medicine
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    ABSTRACT: BACKGROUND Non-alcoholic fatty liver (NAFL) includes a spectrum of diseases ranging from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. NAFL is typically seen in association with obesity, diabetes and hypertriglyceridaemia. In order to seek the role of diet therapy in treatment of NAFL, we compared the ultrasonographic findings of patients with fatty liver disease before and after standard diet therapy. METHODS Twenty-three overweight or obese subjects with incidental fatty liver discovered during ultrasonography were included. Subjects underwent 3 months of diet therapy, and anthropometric data including weight, height, BMI, waist circumference, and hip circumference were measured. Ultrasonographic findings were graded from 0 to 3. Changes in ultrasonographic findings and anthropometric data were studied. RESULTS After three months of dieting, the ultrasonographic grade of all patients decreased by one or two grades. Fifteen patients decreased one grade while 8 others decreased by 2 grades. We observed a significant correlation between the decrease in ultrasonographic grade and the decrease in weight and BMI. CONCLUSION Our study indicates that standard diet therapy could be used as an effective treatment for NAFL patients.
    Full-text · Article · Jan 2010 · Middle East journal of digestive diseases
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    ABSTRACT: Aim: The objective of this review was to assess the effectiveness of diet interventions for improving disease severity in non-alcoholic fatty liver disease. A secondary aim was to identify the effectiveness of different methods of dietetic service delivery for achieving weight reduction in this patient group. Methods: A review of studies from 1999 to 2009 was conducted. Studies were included if they reported non-alcoholic fatty liver disease diagnosis by either liver histology analysis, imaging or by persistent hypertransaminasaemia, were English language studies of human adults, ≥18 years, that had implemented a dietary component in the intervention. Results: From the 102 papers identified, 20 met inclusion criteria: two randomised controlled trials, two controlled trials (allocation method not disclosed), two non-randomised experimental studies and 14 case series. Methods of diet prescription differed substantially among studies. Weight reduction appeared to be associated with a reduction in steatosis; however, improvements in other features of liver disease remain unclear. There appeared to be a relationship between the intensity of dietetic contact and weight loss. Conclusion: There is limited evidence available to assess the effectiveness of diet interventions on histological severity of non-alcoholic fatty liver disease. There is good evidence that clinically significant weight reduction can improve steatosis and risk factors for non-alcoholic fatty liver disease. A relationship may exist between the frequency of dietetic consultations and amount of weight reduction achieved in patients with non-alcoholic fatty liver disease. Fortnightly intervention for a minimum of three months to achieve at least 5% weight loss is recommended.
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