Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss

Dixon, John; Bhathal, Prithi S.; Hughes, Norman R.; O'Brien, Paul Edmond

doi:10.1002/hep.20251

Cited by 689 publications

(459 citation statements)

References 35 publications

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“…Homeostasis model assessment-insulin resistance was calculated (HOMA-IR=[fasting glucose (mmol/L)×fasting insulin (µU/ml)]/22.5) (Bonora et al, 2000). Pathological changes (including steatosis and inflammation) were analyzed by semiquantitative method according to standards proposed by Dixon et al(2004) (Table 1).…”

Section: Methodsmentioning

confidence: 99%

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats

Zhang

et al. 2006

J. Zhejiang Univ. - Sci. B

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Abstract:Objective: The prevalence of non-alcoholic fatty liver disease (NAFLD) has markedly increased. Insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone (PGZ) acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding. Methods: The rats were separated randomly into 6 groups: model group I were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/(kg⋅d) simultaneously, while control group I were fed normal food for 8 weeks; model group II were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/(kg⋅d) orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group II were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), tumor necrosis factor alpha (TNF-α), fasting blood glucose (FBG), fasting plasma insulin (FINS), HOMA (homeostasis model assessment) insulin resistance index (HOMA-IR), and the liver histology of rats of all groups were assayed. Results: After 8 weeks, the liver in model group I showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-α were significantly increased (P<0.05) compared with control group I. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased (P<0.05) compared with model group I. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group II rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels of ALT, AST, ALP, FINS and HOMA-IR were significantly increased (P<0.05) in model group II compared with control group II. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-α and HOMA-IR were significantly decreased compared with model group II. Conclusion: Insulin resistance plays a role in the pathogenesis of NAFLD in rats. Pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.

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Section: Methodsmentioning

confidence: 99%

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats

Zhang

et al. 2006

J. Zhejiang Univ. - Sci. B

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“…Since insulin resistance has been regarded as a risk factor for the progression of liver disease and, moreover, preliminary observations in patients with NASH have shown improvement in liver histology following body weight loss or treatment with insulin sensitizing agents [85][86][87]; further research is needed to disclose the specific role of insulin resistance in CLD. To define the specific roles played by TNF-α and acquired GH resistance in the impairment of glucose metabolism, prospective studies on a large series of patients with CLD are also warranted, grouping patients according to the various aetiologies to better discriminate the effects of aetiologic factors with respect to tissue injury.…”

Section: Discussionmentioning

confidence: 99%

Diabetes in chronic liver disease: from old concepts to new evidence

Picardi

D’Avola

Gentilucci

et al. 2006

Diabetes Metab. Res. Rev.

102

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SummaryThe liver is one of the principal organs involved in glucose metabolism together with skeletal muscle and adipose tissue. A link between diabetes and chronic liver disease (CLD) was first observed in the early half of the last century, but to date several questions remain unsolved. Altered glucose tolerance has been well described in alcoholic CLD, non-alcoholic fatty liver disease, chronic hepatitis C and portal hypertension. Moreover, insulin resistance is assuming an ever-growing importance in CLD; chronic hepatitis C has recently been proposed as a metabolic disease and insulin sensitivity as a predictive factor for liver fibrosis.CLD is also complicated by acquired growth hormone (GH) resistance, characterized by low concentrations of insulin-like growth factor-1 (IGF-1) with respect to normal or elevated GH levels. GH resistance in CLD is determined by several factors, including malnutrition, impaired liver function and reduced expression of hepatic GH receptors. We recently described the possible role of tumour necrosis factor-alpha (TNF-α) in blunting the hepatic response to GH in patients with chronic hepatitis C. The role of GH in impaired glucose metabolism is well known, and recent evidence suggests a receptor and/or post-receptor modulation of insulin signalling. Moreover, as in other chronic inflammatory conditions, pro-inflammatory cytokines may directly modulate the signal cascade that follows insulin binding to its receptor in the course of CLD.In this review, the proposed links between impaired glucose tolerance and CLD are analysed, special emphasis being focussed on the most recent findings concerning the interplay of chronic inflammation, GH resistance and insulin resistance.

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“…[34][35][36][37][38][39][40][41][42] The largest adolescent series to date is also Australian, consisting of 41 adolescents (age range 12-19 years) with a mean weight of 125 kg, and a mean BMI 42 kg/m 2 . 43 These patients generally presented without any major physical health problem associated with obesity, with the exception of five patients with either T2DM, OSAS or hypertension.…”

Section: The Modern Era Of Bariatric Surgical Procedures For Adolescentsmentioning

confidence: 99%

“…Several studies in adults have reported improvement in NAFLD and NASH after surgery, though some studies have highlighted a transient increase in inflammation after surgery. 34,121 Two recent studies of outcome of NASH after bariatric surgery in adults have demonstrated significant decreases in steatosis, but variable or no changes in inflammation and fibrosis. 128,129 Although both of these recent studies in adults suggest a clear beneficial effect of gastric bypass surgery on NAFLD and NASH, the persistence of fibrosis and inflammation in a subset of patients indicate the need for longer-term followup.…”

Section: Nafld and Steatohepatitismentioning

confidence: 99%

Bariatric surgery for pediatric extreme obesity: now or later?

2006

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Obesity is a multifactorial disease of epidemic and global proportions that poses the most significant threat to the health of our younger generations. Those who are the most extremely affected bear the largest burden of health problems. In the US, extreme obesity affects approximately 9 million adults and 2 million children, and is associated with both immediate health problems and later health risk, including premature mortality. Present medical and behavioral interventions for extreme obesity in adults and children rarely result in the significant, durable weight loss necessary to improve health outcomes, prompting a search for more aggressive measures. Weight loss (bariatric) surgery has been advocated as an intervention for those with extreme obesity. In adults, bariatric surgery results in prolonged weight control and improvement in serious obesity comorbidities, namely type 2 diabetes, dyslipidemias, hypertension and obstructive sleep apnea syndrome. A surge in weight loss operations for adolescents has been observed recently, with a threefold increase in case volumes nationwide from 2000 to 2003. Current evidence suggests that after bariatric surgery, adolescents lose significant weight and serious obesity-related medical conditions and psychosocial status are improved. Thus it is reasonable to propose that bariatric surgery performed in the adolescent period may be more effective treatment for childhood-onset extreme obesity than delaying surgery for extremely obese youth until adulthood. This position has been echoed by a number of groups and an independent systematic review. Finally, it is conceivable that bariatric surgery performed in adulthood for childhood onset extreme obesity may not be as effective for comorbidity treatment as surgery performed earlier during adolescence. The purpose of this review is to examine the evidence, which supports early rather than later use of bariatric surgery in the treatment of extreme obesity, and to present this information in light of the medical and surgical risks of bariatric surgery.

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Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss

Cited by 689 publications

References 35 publications

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats

Research on the protection effect of pioglitazone for non-alcoholic fatty liver disease (NAFLD) in rats

Diabetes in chronic liver disease: from old concepts to new evidence

Bariatric surgery for pediatric extreme obesity: now or later?

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