Surgical implantation of adipose tissue reverses diabetes in lipoatrophic mice

Гаврилова, Оксана; Marcus‐Samuels, Bernice; Graham, David; Kim, Jason K.; Shulman, Gerald I.; Castle, Arthur L.; Vinson, Charles; Eckhaus, Michael; Reitman, Marc L.

doi:10.1172/jci7901

Cited by 584 publications

(424 citation statements)

References 32 publications

(20 reference statements)

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“…Moreover, studies on athletes have estimated that for a healthy physiology, the minimal AT amount is 3 % for men and 12 % for women (Measuring and Evaluating Body Composition). In conclusion, the absence of adipocytes is metabolically detrimental (Gavrilova et al 2000).…”

Section: Adipose Tissue and Obesitymentioning

confidence: 90%

“…Studies on mice have shown that life without white AT is possible, but it brings serious physiological consequences such as insulin resistance, diabetes, reduced leptin levels, and early death (Moitra et al 1998). The importance of AT was shown with the use of a mouse model of lipoatrophic diabetes (Gavrilova et al 2000). Fat tissue transplantation from healthy mice into lipoatrophic mice resulted in a dramatic reversal of the hyperglycemia, accompanied by improved muscle insulin sensitivity, lowered insulin concentrations, and decreased amounts of fat deposition in muscle.…”

Section: Adipose Tissue and Obesitymentioning

confidence: 99%

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Obesity and related consequences to ageing

Jura

Kozak

2016

AGE

295

170

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Obesity has become a major public health problem. Given the current increase in life expectancy, the prevalence of obesity also raises steadily among older age groups. The increase in life expectancy is often accompanied with additional years of susceptibility to chronic ill health associated with obesity in the elderly. Both obesity and ageing are conditions leading to serious health problems and increased risk for disease and death. Ageing is associated with an increase in abdominal obesity, a major contributor to insulin resistance and the metabolic syndrome. Obesity in the elderly is thus a serious concern and comprehension of the key mechanisms of ageing and age-related diseases has become a necessary matter. Here, we aimed to identify similarities underlying mechanisms related to both obesity and ageing. We bring together evidence that age-related changes in body fat distribution and metabolism might be key factors of a vicious cycle that can accelerate the ageing process and onset of age-related diseases.

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Section: Adipose Tissue and Obesitymentioning

confidence: 90%

Section: Adipose Tissue and Obesitymentioning

confidence: 99%

Obesity and related consequences to ageing

Jura

Kozak

2016

AGE

295

170

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“…2 Like excessive adiposity, impaired adipogenesis is associated with insulin resistance, 3 and insufficient adipose tissue causes glucose intolerance, which could be reversed by the presence of adipose tissue. [4][5][6] On the other hand, adequate lipid storage in the adipose tissue, 7 or induction of adipogenesis improves insulin sensitivity. [8][9][10] Therefore, understanding the regulation of adipocyte differentiation by cellular and extracellular factors is crucial for better management of chronic conditions such as obesity, insulin resistance and lipodystrophy.…”

Section: Introductionmentioning

confidence: 99%

Human adenovirus Ad-36 induces adipogenesis via its E4 orf-1 gene

et al. 2007

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Objective: Understanding the regulation of adipocyte differentiation by cellular and extracellular factors is crucial for better management of chronic conditions such as obesity, insulin resistance and lipodystrophy. Experimental infection of rats with a human adenovirus type 36 (Ad-36) improves insulin sensitivity and promotes adipogenesis, reminiscent of the effect of thiozolinediones. Therefore, we investigated the role of Ad-36 as a novel regulator of the adipogenic process. Design and Results: Even in the absence of adipogenic inducers, infection of 3T3-L1 preadipocytes and human adipose-derived stem cells (hASC) by Ad-36, but not Ad-2 that is another human adenovirus, modulated regulatory points that spanned the entire adipogenic cascade ranging from the upregulation of cAMP, phosphatidylinositol 3-kinase and p38 signaling pathways, downregulation of Wnt10b expression, and increased expression of CCAAT/enhancer binding protein-b and peroxisome proliferator-activated receptor g2 and consequential lipid accumulation. Next, we identified that E4 open reading frame (orf)-1 gene of the virus is necessary and sufficient for Ad-36-induced adipogenesis. Selective knockdown of E4 orf-1 by RNAi abrogated Ad-36-induced adipogenic signaling cascade in 3T3-L1 cells and hASC. Compared to the null vector, selective expression of Ad-36 E4 orf-1 in 3T3-L1 induced adipogenesis, which was abrogated when the PDZ-binding domain of the protein was deleted. Conclusion: Thus, Ad-36 E4 orf-1 is a novel inducer of rodent and human adipocyte differentiation process.

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“…Paradoxically, a deficiency of adipose tissue, as in lipodystrophy or lipoatrophy in humans [6,7] and rodents [8,9,10], is also associated with insulin resistance. These observations suggest that adipose tissue in health is carrying out some active function that maintains normal insulin sensitivity.…”

mentioning

confidence: 99%