脂肪細胞には、P2Y14受容体という受容体があり、それは、褐色脂肪細胞と繋がっているものです。その受容体を、特異的に攻撃する、焼き切る（Ablationする）、ことで、肥満を改善できる、のではないだろうか、という動物実験の研究発表が、アメリカ糖尿病学会2020で、発表されていました。

1705-P — 2020 ADA
Adipocyte Specific Ablation of P2Y14R Improves Glucose Metabolism in Mice with Diet-Induced Obesity

こういう発見から、新しい抗肥満薬ができるといいですね。

確か、昨年のアメリカ糖尿病学会2019では、十二指腸粘膜を焼き切る（Ablationする）事で、高血糖を防ぐ（ただし肥満は改善しない）という治療法が発表されていました。

この、Ablationという用語は、アメリカ糖尿病学会2020、でも、何回となく見かけます。そして、今年は、とうとう、細胞レベルにまで、たっした用語になっていました。そして、ターゲットは、肥満になっていました。

以下、引用です。

Adipose tissue is one of the major tissues in body regulating glucose and energy homeostasis. White adipose tissue (iWAT) serves as primary site of energy storage while brown (BAT) and beige AT play a major role in energy expenditure. AT also exerts endocrine effects by secreting various adipokines/batokines regulating whole body glucose metabolism. Diverse G protein-coupled receptors (GPCRs) are expressed in adipocytes and thus have emerged as potential targets for novel antidiabetic drugs. P2Y purinergic receptors are a class of GPCRs activated by nucleotides and nucleotide sugars. The purinergic P2Y14 receptor (P2Y14R) is natively activated by UDP-glucose. P2Y14R is expressed in white as well as brown adipocytes, and receptor mRNA levels was increased in iWAT due to high fat feeding. The potential role of P2Y14R in AT with respect to maintaining whole body glucose homeostasis remains unexplored. To this end, we generated a knockout mouse model lacking P2Y14R selectively in adipocytes (Ad-P2Y14-KO) using Cre/loxP technology. Interestingly, Ad-P2Y14-KO consuming a high fat diet gained less weight than the control mice. Body composition revealed that the decrease in body weight gain in Ad-P2Y14-KO was due to a decrease in fat mass. Decreased body weight resulted in improved glucose tolerance and insulin sensitivity in Ad-P2Y14-KO. Moreover, fasting blood glucose and fed plasma insulin levels were decreased in Ad-P2Y14-KO. Circulating levels of adipokines such as leptin were decreased in knockout mice, indicating increased sensitivity to leptin in Ad-P2Y14-KO. Interestingly, a lack of P2Y14R signaling increased lipolysis in adipocytes, as plasma free fatty acids levels was elevated in Ad-P2Y14-KO in the fasting state. Liver weight was decreased in Ad-P2Y14-KO indicating a lack of ectopic deposition of fat due to enhanced lipolysis. Mechanistic studies are underway to link the observed phenotype with P2Y14R signaling in adipocytes.