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饮食诱导的肥胖对年轻和老年小鼠脂肪组织和巨噬细胞炎症反应有不同的影响。

Diet-induced obesity has a differential effect on adipose tissue and macrophage inflammatory responses of young and old mice.

机构信息

Nutritional Immunology Laboratory, JM USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.

出版信息

Biofactors. 2013 May-Jun;39(3):326-33. doi: 10.1002/biof.1075. Epub 2013 Jan 24.

Abstract

Obesity and aging are both associated with increased inflammation in adipose tissue. In this study, we investigated effect of diet-induced obesity on inflammatory status in young and old mice. Young (2 months) and old (19 months) C57BL/6 mice were fed a low-fat (10%, LF) or high-fat (60%, HF) diet for 4.5 months. Adipose tissue from old/LF mice expressed higher levels of IL-1β, IL-6, TNFα, and cyclooxygenase-2 mRNA compared with young/LF mice. HF diet upregulated expression of all these inflammatory markers in young mice to the levels seen in the aged. Adipocytes, but not stromal vascular cells, from old/LF mice produced more IL-6, TNFα, and prostaglandin (PG)E2 than those from young/LF mice. HF diet resulted in an increase of all these markers produced by adipocytes in young, but only TNFα in old mice. PGE2 produced by peritoneal macrophages (Mϕ's) was upregulated with aging, and HF diet induced more IL-6, TNFα, and PGE2 production in young but not in old mice. Thus, HF diet/obesity induces an inflammatory state in both visceral fat cells and peritoneal Mϕ's of young mice, but not so in old mice. Together, these results suggest that HF diet-induced obesity may speed up the aging process as characterized by inflammatory status. This study also indicates that animals have a differential response, depending on their ages, to HF diet-induced obesity and inflammation. This age-related difference in response to HF diet should be considered when using inflammation status as a marker in investigating adverse health impacts of HF diet and obesity.

摘要

肥胖和衰老均与脂肪组织炎症增加有关。在这项研究中,我们研究了饮食诱导的肥胖对年轻和年老小鼠炎症状态的影响。将年轻(2 个月)和年老(19 个月)C57BL/6 小鼠分别用低脂(10%,LF)或高脂(60%,HF)饮食喂养 4.5 个月。与年轻/LF 小鼠相比,年老/LF 小鼠的脂肪组织中 IL-1β、IL-6、TNFα 和环氧化酶-2 mRNA 的表达水平更高。HF 饮食使年轻小鼠的所有这些炎症标志物的表达上调至与老年小鼠相同的水平。与年轻/LF 小鼠相比,来自年老/LF 小鼠的脂肪细胞而非基质血管细胞产生更多的 IL-6、TNFα 和前列腺素(PG)E2。HF 饮食导致年轻小鼠的所有这些标记物的产生增加,但仅导致老年小鼠的 TNFα 增加。腹腔巨噬细胞(Mϕ's)产生的 PGE2 随年龄增长而上调,HF 饮食诱导年轻但不诱导老年小鼠产生更多的 IL-6、TNFα 和 PGE2。因此,HF 饮食/肥胖症在年轻小鼠的内脏脂肪细胞和腹腔 Mϕ's 中诱导炎症状态,但在老年小鼠中则不然。这些结果表明,HF 饮食诱导的肥胖症可能会加速炎症状态的衰老过程。本研究还表明,动物对 HF 饮食诱导的肥胖症和炎症的反应存在差异,具体取决于其年龄。在研究 HF 饮食和肥胖症对健康的不利影响时,应考虑这种与年龄相关的对 HF 饮食诱导的肥胖症和炎症的反应差异。

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