Comparison of proliferation and differentiation capacity of human adipocyte precursor cells from the omental and subcutaneous adipose tissue depot of obese subjects

Harmelen, Vanessa van; Röhrig, K.; Hauner, Hans

doi:10.1016/j.metabol.2003.11.012

Cited by 235 publications

(149 citation statements)

References 18 publications

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“…Limited SC expandability may not only cause ectopic and visceral fat deposition, it could also underlie the higher level of adipose tissue macrophage infiltration in visceral compared with SC fat in the majority of patients with obesity [30,31,35]. In this context, different capacity of preadipocytes from SC and visceral fat depots for adipogenesis together with a typically lower adipogenic and angiogenic potential in obesity may determine the fat-depot difference in the susceptibility for macrophage infiltration [52,53]. Further evidence that limited SC expandability contributes to adipose tissue inflammation and insulin resistance comes from studies in patients with inherited lipodystrophic syndromes.…”

Section: Initial Mechanisms For the Activation Of Adipose Tissue Inflmentioning

confidence: 99%

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

2016

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The worldwide obesity epidemic has become a major health concern, because it contributes to higher mortality due to an increased risk for noncommunicable diseases including cardiovascular diseases, type 2 diabetes, musculoskeletal disorders and some cancers. Insulin resistance may link accumulation of adipose tissue in obesity to metabolic diseases, although the underlying mechanisms are not completely understood. In the past decades, data from human studies and transgenic animal models strongly suggested correlative, but also causative associations between activation of proinflammatory pathways and insulin resistance. Particularly chronic inflammation in adipose tissue seems to play an important role in the development of obesity-related insulin resistance. On the other hand, adipose tissue inflammation has been shown to be essential for healthy adipose tissue expansion and remodelling. However, whether adipose tissue inflammation represents a consequence or a cause of impaired insulin sensitivity remains an open question. A better understanding of the molecular pathways linking excess adipose tissue storage to chronic inflammation and insulin resistance may provide the basis for the future development of anti-inflammatory treatment strategies to improve adverse metabolic consequences of obesity. In this review, potential mechanisms of adipose tissue inflammation and how adipose tissue inflammation may cause insulin resistance are discussed.

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Section: Initial Mechanisms For the Activation Of Adipose Tissue Inflmentioning

confidence: 99%

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

2016

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“…It has been reported that liposuction side and liposuction procedure influences the cell yield, proliferation capacity and frequency of isolated stromal cells [57,[67][68][69][70] , but it is unclear whether this promotes different subpopulations in the isolates.…”

Section: Specific Differences and Culture Standardizationmentioning

confidence: 99%

Adipose-derived mesenchymal stromal/stem cells: An update on their phenotype in vivo and in vitro

Baer¹

2014

WJSC

155

123

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Adipose tissue is a rich, ubiquitous and easily accessible source for multipotent stromal/stem cells and has, therefore, several advantages compared to other sources of mesenchymal stromal/stem cells. Several studies have tried to identify the origin of the stromal/stem cell population within adipose tissue in situ. This is a complicated attempt because no marker has currently been described which unambiguously identifies native adipose-derived stromal/stem cells (ASCs). Isolated and cultured ASCs are a non-uniform preparation consisting of several subsets of stem and precursor cells. Cultured ASCs are characterized by their expression of a panel of markers (and the absence of others), whereas their in vitro phenotype is dynamic. Some markers were expressed de novo during culture, the expression of some markers is lost. For a long time, CD34 expression was solely used to characterize haematopoietic stem and progenitor cells, but now it has become evident that it is also a potential marker to identify an ASC subpopulation in situ and after a short culture time. Nevertheless, long-term cultured ASCs do not express CD34, perhaps due to the artificial environment. This review gives an update of the recently published data on the origin and phenotype of ASCs both in vivo and in vitro. In addition, the composition of ASCs (or their subpopulations) seems to vary between different laboratories and preparations. This heterogeneity of ASC preparations may result from different reasons. One of the main problems in comparing results from different laboratories is the lack of a standardized isolation and culture protocol for ASCs. Since many aspects of ASCs, such as the differential potential or the current use in clinical trials, are fully described in other recent reviews, this review further updates the more basic research issues concerning ASCs' subpopulations, heterogeneity and culture standardization.

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“…Moreover, age is negatively correlated to subcutaneous stromal preadipocyte cell differentiation (van Harmelen et al 2004) possibly due to a loss in nucleotide excision repair enzymes Cockayne syndrome A and B, enhanced mutation rate and subsequent cell loss by apoptosis diminishing depot size (Berneburg 2010). The changes in maturation and differentiation of both the visceral and subcutaneous adipose depots, i.e.…”

Section: Altered Adipocyte Function In Ageingmentioning

confidence: 99%

Ageing, adipose tissue, fatty acids and inflammation

2014

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A common feature of ageing is the alteration in tissue distribution and composition, with a shift in fat away from lower body and subcutaneous depots to visceral and ectopic sites. Redistribution of adipose tissue towards an ectopic site can have dramatic effects on metabolic function. In skeletal muscle, increased ectopic adiposity is linked to insulin resistance through lipid mediators such as ceramide or DAG, inhibiting the insulin receptor signalling pathway. Additionally, the risk of developing cardiovascular disease is increased with elevated visceral adipose distribution.In ageing, adipose tissue becomes dysfunctional, with the pathway of differentiation of preadipocytes to mature adipocytes becoming impaired; this results in dysfunctional adipocytes less able to store fat and subsequent fat redistribution to ectopic sites. Low grade systemic inflammation is commonly observed in ageing, and may drive the adipose tissue dysfunction, as proinflammatory cytokines are capable of inhibiting adipocyte differentiation. Beyond increased ectopic adiposity, the effect of impaired adipose tissue function is an elevation in systemic free fatty acids (FFA), a common feature of many metabolic disorders. Saturated fatty acids can be regarded as the most detrimental of FFA, being capable of inducing insulin resistance and inflammation through lipid mediators such as ceramide, which can increase risk of developing atherosclerosis. Elevated FFA, in particular saturated fatty acids, maybe a driving factor for both the increased insulin resistance, cardiovascular disease risk and inflammation in older adults.

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Comparison of proliferation and differentiation capacity of human adipocyte precursor cells from the omental and subcutaneous adipose tissue depot of obese subjects

Cited by 235 publications

References 18 publications

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?

Adipose-derived mesenchymal stromal/stem cells: An update on their phenotype in vivo and in vitro

Ageing, adipose tissue, fatty acids and inflammation

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