Key result
Brown fat lipoatrophy accelerates atherosclerosis in mice, increasing lesion size and macrophage infiltration.
Why the study?
The impact of severe brown fat lipoatrophy on the atherosclerotic process and associated metabolic and vascular alterations was not well understood.
Does severe brown fat lipoatrophy aggravate the atherosclerotic process in ApoE(-/-) male mice?
Does severe brown fat lipoatrophy aggravate the atherosclerotic process in ApoE(-/-) male mice?
Severe brown fat lipoatrophy aggravates the atherosclerotic process and metabolic dysfunction in ApoE(-/-) mice, highlighting the protective potential of brown adipose tissue activation against obesity-associated vascular damage.
Answers are grounded in this paper and cite their sources.
Brown fat may protect against atherosclerosis; hypothesis-generating in ApoE(-/-) mice, with no direct clinical implications.
Obesity is one of the major risk factors for the development of cardiovascular diseases and is characterized by abnormal accumulation of adipose tissue, including perivascular adipose tissue (PVAT). However, brown adipose tissue (BAT) activation reduces visceral adiposity. To demonstrate that severe brown fat lipoatrophy might accelerate atherosclerotic process, we generated a new mouse model without insulin receptor (IR) in BAT and without apolipoprotein (Apo)E (BAT-specific IR knockout [BATIRKO];ApoE(-/-) mice) and assessed vascular and metabolic alterations associated to obesity. In addition, we analyzed the contribution of the adipose organ to vascular inflammation. Brown fat lipoatrophy induces visceral adiposity, mainly in gonadal depot (gonadal white adipose tissue [gWAT]), severe glucose intolerance, high postprandial glucose levels, and a severe defect in acute insulin secretion. BATIRKO;ApoE(-/-) mice showed greater hypertriglyceridemia than the obtained in ApoE(-/-) and hypercholesterolemia similar to ApoE(-/-) mice. BATIRKO;ApoE(-/-) mice, in addition to primary insulin resistance in BAT, also showed a significant decrease in insulin signaling in liver, gWAT, heart, aorta artery, and thoracic PVAT. More importantly, our results suggest that severe brown fat lipoatrophy aggravates the atherosclerotic process, characterized by a significant increase of lipid depots, atherosclerotic coverage, lesion size and complexity, increased macrophage infiltration, and proinflammatory markers expression. Finally, an increase of TNF-α and leptin as well as a decrease of adiponectin by BAT, gWAT, and thoracic PVAT might also be responsible of vascular damage. Our results suggest that severe brown lipoatrophy aggravates atherosclerotic process. Thus, BAT activation might protect against obesity and its associated metabolic alterations.
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Gómez‐Hernández et al. (2016) studied Atherosclerosis. Severe brown fat lipoatrophy (BAT-specific IR knockout) vs. ApoE(-/-) mice was evaluated on Atherosclerotic process (lipid depots, atherosclerotic coverage, lesion size and complexity). Severe brown fat lipoatrophy in male ApoE(-/-) mice aggravates the atherosclerotic process, characterized by increased lipid depots, lesion size, and macrophage infiltration.
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