The Evolution of Severe Steatosis After Bariatric Surgery Is Related to Insulin Resistance

Mathurin, Philippe; Gonzalez, Florent; Kerdraon, Olivier; Leteurtre, Emmanuelle; Arnalsteen, Laurent; Hollebecque, Antoine; Louvet, Alexandre; Dharancy, Sébastien; Cocq, Perrine; Jany, T.; Boitard, J.; Deltenre, Pierre; Romon, Monique; Pattou, François

doi:10.1053/j.gastro.2006.02.024

Cited by 139 publications

(83 citation statements)

References 51 publications

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“…Attention should now shift from considering hepatic steatosis as a benign process to an important unhealthy condition, which leads to IR, oxidative stress and further progression of NAFLD. This is evident from the fact that severe forms of NASH correlate well with presence of hepatic steatosis, visceral obesity and MS [89] .…”

Section: Two Hit Hypothesismentioning

confidence: 96%

Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease

Qureshi

Abrams

2007

WJG

218

160

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Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized cause of liver-related morbidity and mortality. It can develop secondary to numerous causes but a great majority of NAFLD cases occur in patients who are obese or present with other components of metabolic syndrome (hypertension, dyslipidemia, diabetes). This is called primary NAFLD and insulin resistance plays a key role in its pathogenesis. Obesity is characterized by expanded adipose tissue, which is under a state of chronic inflammation. This disturbs the normal storage and endocrine functions of adipose tissue. In obesity, the secretome (adipokines, cytokines, free fatty acids and other lipid moieties) of fatty tissue is amplified, which through its autocrine, paracrine actions in fat tissue and systemic effects especially in the liver leads to an altered metabolic state with insulin resistance (IR). IR leads to hyperglycemia and reactive hyperinsulinemia, which stimulates lipid-accumulating processes and impairs hepatic lipid metabolism. IR enhances free fatty acid delivery to liver from the adipose tissue storage due to uninhibited lipolysis. These changes result in hepatic abnormal fat accumulation, which may initiate the hepatic IR and further aggravate the altered metabolic state of whole body. Hepatic steatosis can also be explained by the fact that there is enhanced dietary fat delivery and physical inactivity. IR and NAFLD are also seen in various lipodystrophic states in contrary to popular belief that these problems only occur due to excessive adiposity in obesity. Hence, altered physiology of adipose tissue is central to development of IR, metabolic syndrome and NAFLD.

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Section: Two Hit Hypothesismentioning

confidence: 96%

Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease

Qureshi

Abrams

2007

WJG

218

160

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“…It is possible that the very low calorie diet that commonly precedes the actual surgical procedure influences NAFLD and even NASH that may have been present. Finally, a large European study has shown that after five years, if insulin resistance has not improved, fibrosis might actually show progression [124] .…”

Section: Bariatric Patientsmentioning

confidence: 99%

Histopathology of Non-Alcoholic Fatty Liver Disease

Brunt

2009

Clinics in Liver Disease

114

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Histological analysis of liver biopsies remains a standard against which other methods of assessment for the presence and amount of hepatic injury due to nonalcoholic fatty liver disease (NAFLD) are measured. Histological evaluation remains the sole method of distinguishing steatosis from advanced forms of NAFLD, i.e. nonalcoholic steatohepatitis (NASH) and fibrosis. Included in the lesions of NAFLD are steatosis, lobular and portal inflammation, hepatocyte injury in the forms of ballooning and apoptosis, and fibrosis. However, patterns of these lesions are as distinguishing as the lesions themselves. Liver injury in adults and children due to NAFLD may have different histological patterns. In this review, the rationale for liver biopsy, as well as the histopathological lesions, the microscopically observable patterns of injury, and the differential diagnoses of NAFLD and NASH are discussed.

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“…An increased metabolic rate might be harmful to healthy but vulnerable hepatocytes that remain in the liver, and worsening of inflammation and fibrosis may occur as observed in some obese patients with NASH undergoing bariatric surgery and rapid weight loss. 29 In this regard, it has to be taken into account that the experimental models used by Cable et al do not exhibit significant inflammation or fibrosis and therefore the effect of MB07811 in this setting remains unknown.…”

mentioning

confidence: 99%

Burning hepatic fat: Therapeutic potential for liver-specific thyromimetics in the treatment of nonalcoholic fatty liver disease

Arrese

2008

Hepatology

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The Evolution of Severe Steatosis After Bariatric Surgery Is Related to Insulin Resistance

Cited by 139 publications

References 51 publications

Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease

Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease

Histopathology of Non-Alcoholic Fatty Liver Disease

Burning hepatic fat: Therapeutic potential for liver-specific thyromimetics in the treatment of nonalcoholic fatty liver disease

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