Surgical removal of visceral fat reverses hepatic insulin resistance.

Barzilai, Nir; She, Li; Liu, Bing Qian; Vuguin, Patricia; Cohen, Pinchas; Wang, Jiali; Rossetti, Luciano

doi:10.2337/diabetes.48.1.94

Cited by 348 publications

(273 citation statements)

References 15 publications

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“…The first notion is supported by findings that intra-abdominal fat mass reduction improves insulin sensitivity in rats [4], whereas implantation of cultured adipocytes into the peritoneal cavity of mice induces insulin resistance [11].…”

Section: Discussionmentioning

confidence: 96%

“…elderly people or patients with certain forms of lipodystrophy) are prone to develop insulin resistance [1,2]. Second, removal of intra-abdominal fat improved insulin sensitivity [3,4], whereas the removal of subcutaneous fat tissue by liposuction in obese humans did not improve insulin action [5]. Thus, the pattern of body fat distribution, especially abdominal fat accumulation, determines insulin sensitivity.…”

Section: Introductionmentioning

confidence: 99%

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Improved glucose tolerance in mice receiving intraperitoneal transplantation of normal fat tissue

2007

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Aims/hypothesis The association between increased (visceral) fat mass, insulin resistance and type 2 diabetes mellitus is well known. Yet, it is unclear whether the mere increase in intra-abdominal fat mass, or rather functional alterations in fat tissue in obesity contribute to the development of insulin resistance in obese patients. Here we attempted to isolate the metabolic effect of increased fat mass by fat tissue transplantation. Methods Epididymal fat pads were removed from male C57Bl6/J mice and transplanted intraperitoneally into male littermates (recipients), increasing the combined perigonadal fat mass by 50% ( p<0.005). At 4 and 8 weeks post-transplantation, glucose and insulin tolerance tests were performed, and insulin, NEFA and adipokines measured. Results Circulating levels of NEFA, adiponectin and leptin were not significantly different between transplanted and sham-operated control mice, while results of the postprandial insulin tolerance test were similar between the two groups. In contrast, under fasting conditions, the mere increase in intra-abdominal fat mass resulted in decreased plasma glucose levels (6.9 ± 0.4 vs 8.1 ± 0.3 mmol/l, p=0.03) and a ∼20% lower AUC in the glucose tolerance test ( p=0.02) in transplanted mice. Homeostasis model assessment of insulin resistance (HOMA-IR) was 4.1±0.4 in transplanted mice (vs 6.2±0.7 in sham-operated controls) ( p=0.02), suggesting improved insulin sensitivity. Linear regression modelling revealed that while total body weight positively correlated, as expected, with HOMA-IR (β: 0.728, p=0.006), higher transplanted fat mass correlated with lower HOMA-IR (β: −0.505, p=0.031). Conclusions/interpretation Increasing intra-abdominal fat mass by transplantation of fat from normal mice improved, rather than impaired, fasting glucose tolerance and insulin sensitivity, achieving an effect opposite to the expected metabolic consequence of increased visceral fat in obesity.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Improved glucose tolerance in mice receiving intraperitoneal transplantation of normal fat tissue

2007

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“…Surgical removal of visceral fat from laboratory rodents has been shown to improve metabolic function, including insulin sensitivity (Barzilai et al ., 1999). Furthermore, reduction of visceral fat by omentectomy produced significant positive and long‐term effects on glucose homeostasis in humans (Thorne et al ., 2002).…”

Section: Discussionmentioning

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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“…65 A recent study reported that surgical removal of visceral fat reverses hepatic insulin resistance. 66 …”

Section: The Association Of Nash With Obesitymentioning

confidence: 99%

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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Surgical removal of visceral fat reverses hepatic insulin resistance.

Cited by 348 publications

References 15 publications

Improved glucose tolerance in mice receiving intraperitoneal transplantation of normal fat tissue

Improved glucose tolerance in mice receiving intraperitoneal transplantation of normal fat tissue

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

Obesity and liver disease

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