Scholarlink

<p>Obesity is often associated with changes in vascular, metabolic, and chronic inflammatory processes resulting in metabolic syndromes. Adipocyte dysfunction causes dyslipidemia, insulin resistance, glucose intolerance, non-alcoholic fatty liver disease (NAFLD), inflammation, and certain cancers. L-PGDS generates PGD<sub>2</sub> and related non-enzymatic degradation products of the PGJ<sub>2</sub> series in adipocytes and is involved in the transportation of lipophilic compounds. However, its precise physiological role in inflammation and metabolic regulation under healthy conditions remains unclear. To elucidate the relationship between L-PGDS, inflammation, and obesity, this review compiled and summarized current findings. Studies in <i>L-PGDS</i> knockout (KO) mice, primarily generated on the <i>C57BL/6</i> genetic background, consistently demonstrate increased insulin resistance, glucose intolerance, dyslipidemia, atherosclerosis, and obesity. <i>L-PGDS</i> KO mice also exhibit adipocyte hypertrophy and increased gene expression associated with lipogenesis. Conversely, overexpression of <i>L-PGDS</i> has been shown to attenuate adipogenesis in cultured adipocytes, sometimes independently of endogenous prostaglandin production. These findings point out the involvement of L-PGDS in the adipogenesis program and related consequences involving the PPARγ signaling pathway. Furthermore, decreased <i>L-PGDS</i> expression and lower plasma levels have been observed in diet-induced obesity models and insulin-resistant 3T3-L1 adipocytes. The expression level of <i>L-PGDS</i> seemed to reflect the inflammatory activity. Collectively, the available evidence suggests that L-PGDS deficiency may contribute to impaired adipose tissue homeostasis and obesity-associated metabolic dysfunction.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Lipocalin-type Prostaglandin D Synthase (L-PGDS) and its Association with Obesity and Inflammation

  • 期刊论文

  • 发表日期：

    2026年6月23日

查看全文
  • Md. Abdur Rahman Ripon,
  • Md. Mahmodul Islam,
  • Md. Monirul Islam,
  • Md. Abdur Rahman,
  • Mohammad Salim Hossain

摘要

Obesity is often associated with changes in vascular, metabolic, and chronic inflammatory processes resulting in metabolic syndromes. Adipocyte dysfunction causes dyslipidemia, insulin resistance, glucose intolerance, non-alcoholic fatty liver disease (NAFLD), inflammation, and certain cancers. L-PGDS generates PGD2 and related non-enzymatic degradation products of the PGJ2 series in adipocytes and is involved in the transportation of lipophilic compounds. However, its precise physiological role in inflammation and metabolic regulation under healthy conditions remains unclear. To elucidate the relationship between L-PGDS, inflammation, and obesity, this review compiled and summarized current findings. Studies in L-PGDS knockout (KO) mice, primarily generated on the C57BL/6 genetic background, consistently demonstrate increased insulin resistance, glucose intolerance, dyslipidemia, atherosclerosis, and obesity. L-PGDS KO mice also exhibit adipocyte hypertrophy and increased gene expression associated with lipogenesis. Conversely, overexpression of L-PGDS has been shown to attenuate adipogenesis in cultured adipocytes, sometimes independently of endogenous prostaglandin production. These findings point out the involvement of L-PGDS in the adipogenesis program and related consequences involving the PPARγ signaling pathway. Furthermore, decreased L-PGDS expression and lower plasma levels have been observed in diet-induced obesity models and insulin-resistant 3T3-L1 adipocytes. The expression level of L-PGDS seemed to reflect the inflammatory activity. Collectively, the available evidence suggests that L-PGDS deficiency may contribute to impaired adipose tissue homeostasis and obesity-associated metabolic dysfunction.