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Endocrine Abstracts (2016) 41 GP137 | DOI: 10.1530/endoabs.41.GP137

1Biomedical Research Laboratory, Endocrinology Department, IBIMA, Malaga, Spain; 2Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition (CIBEROBN), Madrid, Spain; 3Endocrinology Department, Virgen de la Victoria University Hospital, Malaga, Spain.

Objectives: To study for the first time the differences in monocyte/macrophage infiltration, inflammation and adipogenesis in the subcutaneous and visceral adipose tissues of normal-weight subjects who differed in their degree of metabolic syndrome.

Methods: The study included 92 normal-weight subjects who differed in their degree of metabolic syndrome. Anthropometric and biochemical parameters were measured. RNA from subcutaneous and visceral adipose tissues was isolated, and mRNA expression of monocyte/macrophage infiltration (CD68, CD33, ITGAM, CD163, EMR-1, CD206, MerTK, CD64, ITGAX), inflammation (IL6, TNFα, IL10, IL1b, CCL2, CCL3) and adipogenic and lipogenic capacity markers (PPARgamma, FABP4) were measured. Additionally, cells derived from stromal vascular fraction from subcutaneous and visceral adipose tissues were isolated and expanded, and subsequently differentiated with an adipogenic media, measuring the mRNA expression of adipogenesis (PPARgamma, FABP4, ADRP, C/EBPalpha, LPL, LEP).

Results: Our data indicated a different degree of macrophage infiltration between adipose tissues, with a higher monocyte/macrophage infiltration in subcutaneous adipose tissue in metabolically unhealthy normal-weight subjects, while visceral adipose tissue remained almost unaffected. Moreover, adipogenesis function was decreased in patients with the metabolic syndrome in subcutaneous adipose tissue.

Conclusions: An increased macrophage infiltration of adipose tissue and its consequences, such as a decrease in adipogenesis function, may explain why both obese and normal-weight subjects can develop metabolic diseases or remain healthy.

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