Adipocyte Size Threshold Matters: Link with Risk of Type 2 Diabetes and Improved Insulin Resistance After Gastric Bypass

Cotillard, Aurélie; Poitou, Christine; Torcivia, Adriana; Bouillot, Jean‐Luc; Dietrich, Arne; Klöting, Nora; Grégoire, Cécile; Lolmède, Karine; Blüher, Matthias; Clément, Karine

doi:10.1210/jc.2014-1074

Cited by 113 publications

(88 citation statements)

References 18 publications

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“…Adipocyte hypertrophy has been linked to greater reductions in insulin resistance with diet-induced weight loss. 7 In contrast, a separate study correlated increased adipocyte hypertrophy with lesser reductions in insulin resistance after gastric bypass, 8 suggesting that qualitatively different relationships may exist between hypertrophy and non-surgical and surgical weight loss. Few published data correlate changes in weight with preadipocyte frequency.…”

Section: Discussionmentioning

confidence: 97%

Adipocyte hypertrophy-hyperplasia balance contributes to weight loss after bariatric surgery

et al. 2017

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Predictors of weight loss responses are not well-defined. We hypothesized that adipose tissue phenotypic features related to remodeling would be associated with bariatric surgery weight loss responses. Visceral and subcutaneous adipose tissues collected from patients during bariatric surgery were studied with flow cytometry, immunohistochemistry, and QRTPCR, and results correlated with weight loss outcomes. Age, male sex, and a diagnosis of type 2 diabetes were associated with less weight loss. Adipocyte size was increased and preadipocyte frequency was decreased in visceral adipose tissue from diabetic subjects. Decreased adipose tissue preadipocyte frequency was associated with less weight loss in women but not men. These data suggest that phenotypic features of adipose tissue remodeling may predict responses to weight loss interventions.

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Section: Discussionmentioning

confidence: 97%

Adipocyte hypertrophy-hyperplasia balance contributes to weight loss after bariatric surgery

et al. 2017

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“…Furthermore, genetic predisposition for type 2 diabetes associates with adipocyte hypertrophy in non-obese first-degree relatives [29]. Finally, several studies show that enlarged fat cell size confers an increased risk of developing type 2 diabetes [10,11,30]. When these findings are put together it is tempting to speculate that scWAT hypertrophy independent of excess body fat is an important defect, which triggers local inflammation and impaired lipolysis and these, in turn, facilitate the development of type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

Increased fat cell size: a major phenotype of subcutaneous white adipose tissue in non-obese individuals with type 2 diabetes

et al. 2015

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Aims/hypothesis We aimed to elucidate the impact of fat cell size and inflammatory status of adipose tissue on the development of type 2 diabetes in non-obese individuals. Methods We characterised subcutaneous abdominal adipose tissue by examining stromal cell populations by 13 colour flow cytometry, measuring expression of adipogenesis genes in the progenitor cell fraction and determining lipolysis and adipose secretion of inflammatory proteins in 14 non-obese men with type 2 diabetes and 13 healthy controls matched for age, sex, body weight and total fat mass. Results Individuals with diabetes had larger fat cells than the healthy controls but stromal cell population frequencies, adipose lipolysis and secretion of inflammatory proteins did not differ between the two groups. However, in the entire cohort fat cell size correlated positively with the ratio of M1/M2 macrophages, TNF-α secretion, lipolysis and insulin resistance. Expression of genes encoding regulators of adipogenesis and adipose morphology (BMP4, CEBPα [also known as CEBPA], PPARγ [also known as PPARG] and EBF1) correlated negatively with fat cell size. Conclusions/interpretation We show that a major phenotype of white adipose tissue in non-obese individuals with type 2 diabetes is adipocyte hypertrophy, which may be mediated by an impaired adipogenic capacity in progenitor cells. Consequently, this could have an impact on adipose tissue inflammation, release of fatty acids, ectopic fat deposition and insulin sensitivity.

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“…In this chapter we will briefly describe how adipocyte dysfunction is manifested in humans and animals and give a short overview of its causes and consequences with respect to the metabolic disorders mentioned. Adipocyte growth beyond a critical volume is thought to go along with functional impairments (Guilherme et al, 2008) and increased risk of T2D (Cotillard et al, 2014). The volume that can be tolerated without compromising the adipocyte's function appears to depend on individual parameters that have yet to be fully understood.…”

Section: Adipocyte Dysfunction In Metabolic Disorders: Manifestationmentioning

confidence: 99%

The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

Castro

Grune

Speckmann

2016

Biological Chemistry

121

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White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

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Adipocyte Size Threshold Matters: Link with Risk of Type 2 Diabetes and Improved Insulin Resistance After Gastric Bypass

Cited by 113 publications

References 18 publications

Adipocyte hypertrophy-hyperplasia balance contributes to weight loss after bariatric surgery

Adipocyte hypertrophy-hyperplasia balance contributes to weight loss after bariatric surgery

Increased fat cell size: a major phenotype of subcutaneous white adipose tissue in non-obese individuals with type 2 diabetes

The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

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