Liver Pathology and the Metabolic Syndrome X in Severe Obesity

Marceau, Picard; Biron, Simon; Hould, Frédéric‐Simon; Marceau, Simon; Simard, Serge; Thung, Swan N.; Kral, John G.

doi:10.1210/jcem.84.5.5661

Cited by 465 publications

(286 citation statements)

References 26 publications

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“…Liver weight was significantly increased in control mice fed HFD compared to control mice fed STD and Ames dwarf mice fed either HFD or STD ( P < 0.03) (Fig. 1f) possibly reflecting increased lipid deposits in peripheral tissues (Marceau et al ., 1999). The same trend was also observed in pancreas weight ( P < 0.02) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Long‐lived hypopituitary Ames dwarf mice are resistant to the detrimental effects of high‐fat diet on metabolic function and energy expenditure

Hill

Fang

Miquet³

et al. 2016

Aging Cell

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SummaryGrowth hormone (GH) signaling stimulates the production of IGF‐1; however, increased GH signaling may induce insulin resistance and can reduce life expectancy in both mice and humans. Interestingly, disruption of GH signaling by reducing plasma GH levels significantly improves health span and extends lifespan in mice, as observed in Ames dwarf mice. In addition, these mice have increased adiposity, yet are more insulin sensitive compared to control mice. Metabolic stressors such as high‐fat diet (HFD) promote obesity and may alter longevity through the GH signaling pathway. Therefore, our objective was to investigate the effects of a HFD (metabolic stressor) on genetic mechanisms that regulate metabolism during aging. We show that Ames dwarf mice fed HFD for 12 weeks had an increase in subcutaneous and visceral adiposity as a result of diet‐induced obesity, yet are more insulin sensitive and have higher levels of adiponectin compared to control mice fed HFD. Furthermore, energy expenditure was higher in Ames dwarf mice fed HFD than in control mice fed HFD. Additionally, we show that transplant of epididymal white adipose tissue (eWAT) from Ames dwarf mice fed HFD into control mice fed HFD improves their insulin sensitivity. We conclude that Ames dwarf mice are resistant to the detrimental metabolic effects of HFD and that visceral adipose tissue of Ames dwarf mice improves insulin sensitivity in control mice fed HFD.

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Section: Resultsmentioning

confidence: 99%

Long‐lived hypopituitary Ames dwarf mice are resistant to the detrimental effects of high‐fat diet on metabolic function and energy expenditure

Hill

Fang

Miquet³

et al. 2016

Aging Cell

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“…58 The distribution of fatty metamorphosis and fibrosis in the morbidly obese patient may correlate in severity with the degree of impaired glucose tolerance. 69 In the large series of Marceau et al 59 , patients with impaired glucose tolerance or diabetes had a sevenfold increased risk of fibrosis (P < 0.0001). Apart from age, diabetes appears to be a strong independent predictor of severe hepatic fibrosis in NASH.…”

Section: The Association Of Nash With Type 2 Diabetesmentioning

confidence: 95%

“…In 551 liver biopsies, steatosis was found in 86%, fibrosis in 74%, mild inflammation or steatohepatitis in 24%, and unexpected cirrhosis in 2% of the patients. 59 In a large personal series of 528 severely obese subjects (BMI 42.6 + 6.8 kg/m 2 ), 74% of the biopsies showed fatty deposition, estimated as mild in 41% of cases, moderate in 32% and severe in 27%. 60 The severity of steatosis was positively associated with BMI (P = 0.002), but not with the known duration of obesity.…”

Section: The Association Of Nash With Obesitymentioning

confidence: 99%

“…Marceau et al 59 reported on the frequent association between the metabolic syndrome observed in severe obesity and liver pathology in 551 liver biopsies performed during antiobesity surgery. With each addition of one of the four following components of the metabolic syndrome (elevated waist/hip ratio, impaired glucose tolerance, hypertension, and dyslipidaemia), the risk of steatosis increased exponentially from 1-to 99-fold (P < 0.001).…”

Section: The Association Of Nash With Insulin Resistance Syndromementioning

confidence: 99%

See 1 more Smart Citation

Obesity and liver disease

Scheen

Luyckx

2002

Best Practice & Research Clinical Endocrinology & Metab

118

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Non-alcoholic steatohepatitis (NASH) is a disease of emerging identity and importance. It is frequently associated with obesity, especially visceral fat, and is intimately related to fatty liver and markers of the insulin resistance syndrome. Both the prevalence and the severity of liver steatosis are related to body mass index, waist circumference, hyperinsulinaemia, hypertriglyceridaemia and impaired glucose tolerance or type 2 diabetes. The identification of obese patients who may progress from steatosis to NASH and from NASH to fibrosis/cirrhosis is an important clinical challenge. Substantial weight loss is accompanied by a marked attenuation of insulin resistance and related metabolic syndrome and, concomitantly, by a remarkable regression of liver steatosis in most patients, although increased inflammation may be detected in some subjects. Thus, NASH may be considered as another disease of affluence, as is the insulin resistance syndrome, and perhaps being part of it, especially in obese patients.

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“…40 In a series of 551 liver biopsies performed on patients with severe obesity undergoing bariatric surgery, 86% had steatosis, 24% steatohepatitis and 2% cirrhosis. 41 The severity of fatty liver in obese patients positively correlates with body mass index (BMI). 42 Fatty Table 3 The relationship between GGT, obesity and hypertension 27 Baseline GGT (U/l) P for trend Figure 1 Complex interrelationship between the various components of the metabolic syndrome and NAFLD.…”

Section: Hypertension Metabolic Syndrome and Fatty Livermentioning

confidence: 99%