Pathophysiology of Human Visceral Obesity: An Update

Abstract

LTchernof A, Després J-P. Pathophysiology of Human Visceral Obesity: An Update. Physiol Rev 93: 359 -404, 2013; doi:10.1152/physrev.00033.2011.-Excess intra-abdominal adipose tissue accumulation, often termed visceral obesity, is part of a phenotype including dysfunctional subcutaneous adipose tissue expansion and ectopic triglyceride storage closely related to clustering cardiometabolic risk factors. Hypertriglyceridemia; increased free fatty acid availability; adipose tissue release of proinflammatory cytokines; liver insulin resistance and inflammation; increased liver VLDL synthesis and secretion; reduced clearance of triglyceride-rich lipoproteins; presence of small, dense LDL particles; and reduced HDL cholesterol levels are among the many metabolic alterations closely related to this condition. Age, gender, genetics, and ethnicity are broad etiological factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage when facing positive energy balance and weight gain may involve sex hormones, local cortisol production in abdominal adipose tissues, endocannabinoids, growth hormone, and dietary fructose. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity. Thiazolidinediones, estrogen replacement in postmenopausal women, and testosterone replacement in androgen-deficient men have been shown to favorably modulate body fat distribution and cardiometabolic risk to various degrees. However, some of these therapies must now be considered in the context of their serious side effects. Lifestyle interventions leading to weight loss generally induce preferential mobilization of visceral fat. In clinical practice, measuring waist circumference in addition to the body mass index could be helpful for the identification and management of a subgroup of overweight or obese patients at high cardiometabolic risk.

Hemodynamic Correlates of Abnormal Aortic Root Dimension in an Adult Population: The Strong Heart Study

“…Central fat distribution has been reported to be associated with elevated levels of circulating inflammatory markers 31, 32. There are many conditions in which a high inflammatory state has been reported to be associated with AR dilatation,33, 34 thus the correlation between ARD and markers of inflammation, such as neutrophil percentage in the present study, was not a surprise 35.…”

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

“…Subcutaneous and visceral adipose tissues differ by phenotypic, physiological and functional characteristics [43]. Specific differences in inflammatory profile have also been reported, with more macrophages [29,31,33], T lymphocytes [31,33], and inflammatory molecules in the visceral vs the subcutaneous tissues of obese individuals [29,33].…”

“…Furthermore, it is associated with ectopic lipid accumulation in the liver and skeletal muscle, which participates to local insulin resistance and contributes to associated metabolic complications [43]. Subcutaneous and visceral adipose tissues differ by phenotypic, physiological and functional characteristics [43].…”

Une relation « inflammée » entre le complexe GPS2 et le tissu adipeux dans l’obésité

“…Ce fuseau se forme à l'emplacement du noyau, quasiment au centre de la cellule. Chez la souris, cinq à six heures après NEBD, le fuseau migre selon son grand axe vers le cortex le plus proche [1], et, huit à neuf heures après NEBD, une première division asymétrique a lieu avec expulsion d'un premier globule polaire contenant la moitié des chromosomes homologues et une quantité de cytoplasme réduite à son minimum. Le fuseau de deuxième division méiotique se reforme directement excentré et parallèle au cortex.…”

“…L'obésité : une pathologie inflammatoire L'obésité est considérée comme une maladie inflammatoire que caracté-rise une détérioration métabolique et inflammatoire du tissu adipeux [1]. Dans le cadre d'une réponse physiologique, l'inflammation est un mécanisme de défense qui protège l'organisme d'un traumatisme ou d'une infection.…”