The Metabolic Phenotype in Obesity: Fat Mass, Body Fat Distribution, and Adipose Tissue Function

Goossens, Gijs H.

doi:10.1159/000471488

Cited by 6,075 publications

(432 citation statements)

References 62 publications

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“…Adipose tissue dysfunction usually occurs due to pathological expansion of fat mass and/or unhealthy distribution of body fat, resulting in cardiometabolic complications and other related diseases [21-23]. Epidemiological, clinical, and translational studies over the past decades have provided evidence of the strong link between visceral and ectopic fat and the development of dyslipidemia, insulin resistance, hypertension, atherosclerosis, and adverse cardiac remodeling, among others [20].…”

Section: New Advanced Diagnostic Frameworkmentioning

confidence: 99%

“…The functionality of adipose tissue relates to its mechanical and secretory properties, which translate into its expansion capacity as well as secretion pattern of adipokines. In fact, adipose tissue dysfunction is linked to a decreased expandability of adipocytes to accommodate the dietary energy surplus in the form of triglycerides, which seems to be related to alterations in extracellular matrix composition and fibrotic characteristics [26], as well as low-grade chronic inflammation [23]. Together, these impairments have both local and systemic effects [26, 23].…”

Section: New Advanced Diagnostic Frameworkmentioning

confidence: 99%

“…In fact, adipose tissue dysfunction is linked to a decreased expandability of adipocytes to accommodate the dietary energy surplus in the form of triglycerides, which seems to be related to alterations in extracellular matrix composition and fibrotic characteristics [26], as well as low-grade chronic inflammation [23]. Together, these impairments have both local and systemic effects [26, 23]. Thus, an “adiposity-based” diagnosis allows a more specific analysis of complications determined by dysfunctional adipose tissue, based on the preponderance of scientific and clinical evidence [27].…”

Section: New Advanced Diagnostic Frameworkmentioning

confidence: 99%

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The ABCD of Obesity: An EASO Position Statement on a Diagnostic Term with Clinical and Scientific Implications

et al. 2019

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Obesity is a frequent, serious, complex, relapsing, and chronic disease process that represents a major public health problem. The coining of obesity as an adiposity-based chronic disease (ABCD) is of particular relevance being in line with EASO’s proposal to improve the International Classification of Diseases ICD-11 diagnostic criteria for obesity based on three dimensions, namely etiology, degree of adiposity, and health risks. The body mass index as a unique measurement of obesity does not reflect the whole complexity of the disease. Obesity complications are mainly determined by 2 pathological processes, i.e., physical forces (fat mass disease) as well as endocrine and immune responses (sick fat disease), which are embedded in a cultural and physical context leading to a specific ABCD stage.

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Section: New Advanced Diagnostic Frameworkmentioning

confidence: 99%

Section: New Advanced Diagnostic Frameworkmentioning

confidence: 99%

Section: New Advanced Diagnostic Frameworkmentioning

confidence: 99%

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The ABCD of Obesity: An EASO Position Statement on a Diagnostic Term with Clinical and Scientific Implications

et al. 2019

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“…An estimated 10-30% of obese individuals maintain glycemic control and some longitudinal studies suggest their risk of developing type II diabetes is no greater than matched lean individuals (1). No causative factors underlying glycemic control in obesity have been discovered, however the strongest predictors of impaired glycemic control in obesity are increased visceral fat mass and adipose tissue dysfunction (2,3). Thus research efforts have focused on understanding the genetic and physiological mechanisms of action of adipose.…”

Section: Introductionmentioning

confidence: 99%

Brown adipose expansion and remission of glycemic dysfunction in obese SM/J mice

Carson

Macias-Velasco

Gunawardana

et al. 2019

Preprint

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52Disruption of glucose homeostasis increases the risk of type II diabetes, cardiovascular disease, stroke, 53 and cancer. We leverage a novel rodent model, the SM/J mouse, to understand glycemic control in 54 obesity. On a high fat diet, obese SM/J mice initially develop impaired glucose tolerance and elevated 55 fasting glucose. Strikingly, their glycemic dysfunction resolves by 30 weeks of age despite persistence of 56 obesity. A prominent phenotype is that they dramatically expand their brown adipose depots as they 57 resolve glycemic dysfunction. This occurs naturally and spontaneously on a high fat diet, with no 58 temperature or genetic manipulation. When the brown adipose depot is removed from normoglycemic 59 obese mice, fasting blood glucose and glucose tolerance revert to unhealthy levels, and animals become 60 insulin resistant. We identified 267 genes whose expression changes in the brown adipose when the 61 mice resolve their unhealthy glycemic parameters, and find the expanded tissue has a 'healthier' 62 expression profile of cytokines and extracellular matrix genes. We describe morphological, physiological, 63 and transcriptomic changes that occur during the unique brown adipose expansion and remission of 64 glycemic dysfunction in obese SM/J mice. Understanding this phenomenon in mice will open the door for 65 innovative therapies aimed at improving glycemic control in obesity.66 67 Significance Statement 68 Some obese individuals maintain normal glycemic control. Despite being obese, these individuals 69 have low risk for metabolic complications, including type-II diabetes. If we better understood why some 70 obese people maintain normoglycemia then we might develop new approaches for treating metabolic 71 complications associated with obesity. However, the causative factors underlying glycemic control in 72 obesity remain unknown. We discovered that, despite persistence of the obese state, SM/J mice enter 73 into diabetic remission: returning to normoglycemia and reestablishing glucose tolerance and improving 74 insulin sensitivity. A prominent phenotype is that they dramatically expand their brown adipose depots as 75 they resolve glycemic dysfunction. Understanding this phenomenon in mice will open the door for 76 innovative therapies aimed at improving glycemic control in obesity. 78An estimated 10-30% of obese individuals maintain glycemic control and some longitudinal 79 studies suggest their risk of developing type II diabetes is no greater than matched lean individuals (1). 80No causative factors underlying glycemic control in obesity have been discovered, however the strongest 81 predictors of impaired glycemic control in obesity are increased visceral fat mass and adipose tissue 82 dysfunction (2,3). Thus research efforts have focused on understanding the genetic and physiological 83 mechanisms of action of adipose. Recent research reveals that brown adipose activity is associated with 84 anti-diabetic properties. Cold exposure in both obese and lean individuals causes increased uptake...

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“…However, BMI like all anthropometric measurements, although inexpensive and simple to perform, are surrogate measures of body fatness and, especially in some clinical conditions [4], provide misleading information about body fat content. Besides, the use of universal BMI cut-off points to classify subjects as normal weight, overweight and obese, do not consistently reflect adiposity in different ethnic populations [5].…”

Section: Is It Time To Move Beyond Bmi: Body Fat Mass and Distributionmentioning

confidence: 99%

Fat and Lipid Partitioning: Phenotyping Beyond BMI

2017

DEMD

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The world-wide obesity epidemic, predisposing towards several chronic diseases, not only poses a major public health issue, but also has a negative impact on individual' life expectancy and quality. These two dimensions may need distinct diagnostic and preventive approaches. Indeed, whether BMI and total adiposity are positively correlated with cardiometabolic disease risk at the population level, adipose tissue regional distribution and lipid storage in ectopic tissues define the obesity phenotype and, thus, better predict the risk of developing obesity complications at the individual level.Indeed, together with the more extensively studied intraabdominal adipose tissue, smaller ectopic visceral depots have, in the recent years, gained increasing attention for their putative role in mediating the local detrimental effects of obesity. It has also been increasingly appreciated that intracellular lipid accumulation in non-adipose tissues leads to pathological responses and impaired insulin signaling. This narrative review focuses on the phenotypic differences between different adipose depots that link their depotspecific biology to obesity specific complications.

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The Metabolic Phenotype in Obesity: Fat Mass, Body Fat Distribution, and Adipose Tissue Function

Cited by 6,075 publications

References 62 publications

The ABCD of Obesity: An EASO Position Statement on a Diagnostic Term with Clinical and Scientific Implications

The ABCD of Obesity: An EASO Position Statement on a Diagnostic Term with Clinical and Scientific Implications

Brown adipose expansion and remission of glycemic dysfunction in obese SM/J mice

Fat and Lipid Partitioning: Phenotyping Beyond BMI

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