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The color of fat and its central role in the development and progression of metabolic diseases

Academic Article
Publication Date:
2017
abstract:
Excess caloric intake does not always translate to an expansion of the subcutaneous adipose tissue (SAT) and increase in fat mass. It is now recognized that adipocyte type (white, WAT, or brown, BAT), size (large vs. small) and metabolism are important factors for the development of cardiometabolic diseases. When the subcutaneous adipose tissue is not able to expand in response to increased energy intake the excess substrate is stored as visceral adipose tissue or as ectopic fat in tissues as muscle, liver and pancreas. Moreover, adipocytes become dysfunctional (adiposopathy, or sick fat), adipokines secretion is increased, fat accumulates in ectopic sites like muscle and liver and alters insulin signaling, increasing the demand for insulin secretion. Thus, there are some subjects that despite having normal weight have the metabolic characteristics of the obese (NWMO), while some obese expand their SAT and remain metabolically healthy (MHO). In this paper we have reviewed the recent findings that relate the metabolism of adipose tissue and its composition to metabolic diseases. In particular, we have discussed the possible role of dysfunctional adipocytes and adipose tissue resistance to the antilipolytic effect of insulin on the development of impaired glucose metabolism. Finally we have reviewed the possible role of BAT vs. WAT in the alteration of lipid and glucose metabolism and the recent studies that have tried to stimulate browning in human adipose tissue.
Iris type:
01.01 Articolo in rivista
Keywords:
brown adipose tissue; insulin resistance; lipid metabolism; NAFLD
List of contributors:
Carli, Fabrizia; Gastaldelli, Amalia; Gaggini, Melania
Authors of the University:
GAGGINI MELANIA
GASTALDELLI AMALIA
Handle:
https://iris.cnr.it/handle/20.500.14243/341219
Published in:
HORMONE MOLECULAR BIOLOGY AND CLINICAL INVESTIGATION
Journal
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http://www.scopus.com/record/display.url?eid=2-s2.0-85030664372&origin=inward
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