Department of Medicine (H7), C2-94, Karolinska Institutet at Karolinska University Hospital, Huddinge, Stockholm, Sweden.
J Intern Med. 2017 Sep;282(3):220-228. doi: 10.1111/joim.12641. Epub 2017 Jul 12.
Although white adipose tissue mass and distribution correlates with cardiovascular disease, the fat cell-specific perturbations underlying this association are not known. We determined the relationship between adipocyte size and lipid metabolism with cardiovascular risk.
DESIGN/SUBJECTS: Adipocyte size as well as spontaneous (basal) and hormone-stimulated effects on adipocyte lipid metabolism (lipolysis and lipogenesis) were investigated in abdominal subcutaneous adipose tissue of 304 men and 775 women. Subjects were classified into five categories according to Adult Treatment Panel III (ATPIII) metabolic syndrome criteria.
Adipocyte size increased with increasing ATPIII score (P < 0.0001). For lipolysis, there was a gradual increase in basal and catecholamine-stimulated lipolysis and a decrease in insulin-mediated inhibition of stimulated lipolysis with ATPIII (P < 0.0001). In contrast, the lipolytic action of atrial natriuretic peptide was similar between ATPIII classes. Basal and insulin-stimulated lipogenesis decreased with increasing score (P < 0.0001). Circulating free fatty acid levels were 50% higher in the top risk category (4-5) compared with the lowest score (P < 0.0001). Fat cell size correlated positively with increasing ATPIII score and lipolysis but negatively with lipogenesis. All these differences were independent of age, sex and body weight status (P < 0.0001 to 0.02 after correction). When all functional measures were put together, maximum insulin-stimulated lipogenesis, insulin-antilipolytic sensitivity and basal lipolysis together explained about 20% in the variation of ATPIII in score.
Independently of sex, age and body weight status, a high cardiovascular risk score associates with increased circulating free fatty acid levels and hormone-specific alterations of lipolysis/lipogenesis in enlarged subcutaneous fat cells.
尽管白色脂肪组织的质量和分布与心血管疾病相关,但这种关联所涉及的脂肪细胞特异性改变尚不清楚。本研究旨在确定脂肪细胞大小与心血管风险之间的关系。
设计/研究对象:本研究检测了 304 名男性和 775 名女性腹部皮下脂肪中的脂肪细胞大小,以及脂肪细胞脂质代谢(脂肪分解和脂肪生成)的自发性(基础)和激素刺激效应。根据成人治疗组 III(ATPIII)代谢综合征标准,将受试者分为五组。
随着 ATPIII 评分的增加,脂肪细胞大小呈增加趋势(P<0.0001)。对于脂肪分解,基础和儿茶酚胺刺激的脂肪分解逐渐增加,而胰岛素介导的刺激脂肪分解的抑制作用随着 ATPIII 评分的增加而降低(P<0.0001)。相反,心钠肽的脂肪分解作用在 ATPIII 各分类之间相似。基础和胰岛素刺激的脂肪生成随着评分的增加而减少(P<0.0001)。在最高风险类别(4-5)中,循环游离脂肪酸水平比最低评分(P<0.0001)高 50%。脂肪细胞大小与 ATPIII 评分的增加呈正相关,与脂肪生成呈负相关。所有这些差异均独立于年龄、性别和体重状况(校正后 P<0.0001 至 0.02)。当所有功能测量指标放在一起时,最大胰岛素刺激的脂肪生成、胰岛素抗脂肪分解敏感性和基础脂肪分解共同解释了 ATPIII 评分变异的约 20%。
独立于性别、年龄和体重状况,高心血管风险评分与循环游离脂肪酸水平升高以及大脂肪细胞中脂肪分解/脂肪生成的激素特异性改变相关。