The biology of white adipocyte proliferation

Hausman, Dorothy B.; DiGirolamo, Mario; Bartness, Timothy J.; Hausman, Gary; Martin, Roy J.

doi:10.1046/j.1467-789x.2001.00042.x

Cited by 606 publications

(486 citation statements)

References 162 publications

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“…Studies on rodents and humans showed that the body of a healthy, lean individual is composed of approximately 15-28 % fat mass (Avram et al 2005a) with low variance; however, a high-fat diet (HFD) induces obesity with a wide variability of fat mass accumulation as seen in some mouse genotypes (Moitra et al 1998;Hausman et al 2001;Koza et al 2006). Similarly, a wide range of phenotypes occur at the metabolic and functional levels in obese individuals, where excessive AT accumulation may lead to the metabolic syndrome (Kirkland 2013).…”

Section: Adipose Tissue and Obesitymentioning

confidence: 99%

Obesity and related consequences to ageing

Jura

Kozak

2016

AGE

344

203

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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: 99%

Obesity and related consequences to ageing

Jura

Kozak

2016

AGE

344

203

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“…Increased adiposity involves increases in fat-cell size and also new adipocyte formation through adipogenesis. 1,[5][6][7] Thus, a greater understanding of the molecular basis of adipogenesis may suggest rational therapeutic strategies aimed at manipulating adipocyte development as a means of treating disorders of adipose tissue mass.…”

Section: Introductionmentioning

confidence: 99%

The NR4A family of orphan nuclear receptors are not required for adipogenesis

O’Rahilly

et al. 2007

Int J Obes

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Nuclear hormone receptors of the NR4A subfamily are rapidly induced during the early stages of adipogenesis, leading to the speculation that they may have important roles in this process. One of the three subfamily members, Nur77 has also been shown to play key roles in energy expenditure and lipolysis in skeletal muscle and in the control of hepatic gluconeogenesis. We, therefore, examined the role of NR4A factors in adipogenesis using the well-characterized 3T3-L1 preadipocyte model. Inhibition of Nur77 expression using siRNA did not affect induction of adipogenic genes, nor the accumulation of lipid. To inhibit the activity of all the three NR4A family members, we generated preadipocytes stably expressing a well-characterized dominant-negative Nur77 (DN-Nur77), known to block the function of the other NR4A factors, Nurr1 and Nor1, as well as Nur77. While the increased NR4A activity observed following adipogenic induction was completely abolished in these cells, DNNur77 expression did not affect the expression of genes characteristic of terminally differentiated adipocytes and had no impact on lipid accumulation in these cells. Thus, while members of the NR4A subfamily of nuclear receptors may have important metabolic roles in skeletal muscle and liver, we demonstrate that they are dispensable for normal adipocyte development.

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“…However, much less is known about how adipose tissue becomes obese in adult animals. Because the number of adipocytes in a given fat mass increases in obesity (5), adipose tissue obesity is thought to depend on both hypertrophy of preexisting adipocytes and hyperplasia due to formation of new adipocytes from precursor cells (adipogenesis) (5)(6)(7). The adipose tissue stroma contains blood vessels and other cell types.…”

mentioning

confidence: 99%

Adipogenesis in Obesity Requires Close Interplay Between Differentiating Adipocytes, Stromal Cells, and Blood Vessels

et al. 2007

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OBJECTIVE-The expansion of adipose tissue mass seen in obesity involves both hyperplasia and hypertrophy of adipocytes. However, little is known about how adipocytes, adipocyte precursors, blood vessels, and stromal cells interact with one another to achieve adipogenesis. RESEARCH DESIGN AND METHODS-We have developed a confocal microscopy-based method of three-dimensional visualization of intact living adipose tissue that enabled us to simultaneously evaluate angiogenesis and adipogenesis in db/db mice.RESULTS-We found that adipocyte differentiation takes place within cell clusters (which we designated adipogenic/angiogenic cell clusters) that contain multiple cell types, including endothelial cells and stromal cells that express CD34 and CD68 and bind lectin. There were close spatial and temporal interrelationships between blood vessel formation and adipogenesis, and the sprouting of new blood vessels from preexisting vasculature was coupled to adipocyte differentiation. CD34 ϩ CD68 ϩ lectin-binding cells could clearly be distinguished from CD34 Ϫ CD68 ϩ macrophages, which were scattered in the stroma and did not bind lectin. Adipogenic/angiogenic cell clusters can morphologically and immunohistochemically be distinguished from crownlike structures frequently seen in the late stages of adipose tissue obesity. Administration of anti-vascular endothelial growth factor (VEGF) antibodies inhibited not only angiogenesis but also the formation of adipogenic/angiogenic cell clusters, indicating that the coupling of adipogenesis and angiogenesis is essential for differentiation of adipocytes in obesity and that VEGF is a key mediator of that process. CONCLUSIONS-Living tissue imaging techniques providenovel evidence of the dynamic interactions between differentiating adipocytes, stromal cells, and angiogenesis in living obese adipose tissue. Diabetes

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The biology of white adipocyte proliferation

Cited by 606 publications

References 162 publications

Obesity and related consequences to ageing

Obesity and related consequences to ageing

The NR4A family of orphan nuclear receptors are not required for adipogenesis

Adipogenesis in Obesity Requires Close Interplay Between Differentiating Adipocytes, Stromal Cells, and Blood Vessels

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