Hubungan Lingkar Pinggang, Homeostasis Model Assessment of Insulin Resistance, dan Prostaglandin-I2 dengan Test Agregasi Trombosit pada Subyek Obesitas Sentral

Overweight and obese are global health problems and tend to increase in Indonesia. Central obesity is associated with inflammation, insulin resistance, and increased reactive oxidative stress. Insulin resistance can cause a decrease in prostaglandin I2 (PGI2) and nitric oxide (NO) levels, and an increase in platelet aggregation. Its effect in platelet aggregation may increase thrombus formation in blood vessels. This study was aimed to determine the relationship between waist circumference (WC) with HOMA-IR, PGI2 and platelet aggregation test (PAT) in central obese subjects. This was an observational and analytical correlational study with a cross-sectional design conducted at Prof. dr. R. D. Kandou Hospital, Manado. Samples were 33 central obese subjects, 19 were male and 14 were female. Insulin resistance was measured by using HOMA- IR, urine PGI2, and PAT. The Spearmann and Pearson correlation test showed a positive correlation between WC and HOMA-IR (r=0.366, p=0.036). There was a negative correlation but not significant between WC and PGI2 (r=-0.169, p=0.347); between WC and PAT (r=0.094, p=0.603); between HOMA-IR and PGI2 (r=-0.218, p=0.223); and between HOMA-IR and PAT (r=0.080, p=0.658). In conclusion, in central obese people, there is a relationship between WC and HOMA-IR, but there is no relationship between WC, PGI2, and PAT.Keywords: central obesity, HOMA-IR, prostaglandin-I2, platelet aggregation test Abstrak: Berat badan berlebih atau obesitas merupakan masalah kesehatan global dan terus meningkat di Indonesia. Pada obesitas sentral terjadi inflamasi, resistensi insulin, dan mening-katnya reaktif oksidatif stress. Resistensi insulin mampu menyebabkan penurunan kadar prostaglandin I2 (PGI2) dan nitrik oksida (NO). Penurunan kadar PGI2 dapat menyebabkan peningkatan agregasi trombosit yang selanjutnya meningkatkan kemungkinan terjadinya trombus dalam pembuluh darah. Penelitian ini bertujuan untuk mengetahui hubungan antara lingkar pinggang dengan HOMA-IR, PGI2, dan test agregasi trombosit (TAT) pada subyek obes sentral. Jenis penelitian ialah observasional analitik bentuk korelasional dengan desain potong lintang. Penelitian dilakukan di RSUP Prof. dr. R. D. Kandou Manado. Total sampel 33 subyek dengan obesitas sentral, 19 laki-laki dan 14 perempuan. Pengukuran resistensi insulin menggunakan HOMA-IR, PGI2 urin, dan TAT. Uji korelasi Spearmann dan Pearson. mendapatkan korelasi positif antara LP dengan HOMA-IR (r=0,366; p=0,036). Terdapat korelasi negatif tidak bermakna pada hubungan antara LP dengan PGI2 (r=-0,169; p=0,347); hubungan antara LP dengan TAT (r=0,094; p=0,603); hubungan antara HOMA-IR dengan PGI2 (r=-0,218;p=0,223); dan hubungan antara HOMA-IR dengan TAT (r=0,080; p=0,658). Simpulan penelitian ini ialah pada subyek obes sentral terdapat hubungan antara lingkar pinggang dengan HOMA-IR, tetapi tidak terdapat hubungan antara lingkar pinggang dengan PGI2 dan TAT. Kata kunci: obesitas sentral, HOMA-IR, prostaglandin-I2, tes agregasi trombosit

Prostaglandin I2 mediates weak vasodilatation in human placental microvessels

Human placental vessels (HPVs) play important roles in the exchange of metabolites and oxygen in maternal-fetal circulation. Endothelial-derived prostacyclin (prostaglandin I2, PGI2) is a critical endothelial vasodilator in the body. However, the physiological and pharmacological functions of endothelial PGI2 in the human placenta are still unclear. Human, sheep, and rat blood vessels were used in this study. Unlike non-placental vessels (non-PVs), the PGI2 synthesis inhibitor tranylcypromine (TCP) did not modify 5-hydroxytryptamine (5-HT)-induced vascular contraction, indicating that endothelial-derived PGI2 was weak in PVs. Vascular responses to exogenous PGI2 showed slight relaxation followed by a significant contraction at a higher concentration in HPV, which was inhibited by the thromboxane-prostanoid (TP) receptors antagonist SQ-29,548. Testing PVs and non-PVs from sheep also showed similar functional results. More TP receptors than PGI2 (IP) receptors were observed in HPVs. The whole-cell K+ current density of HPVs was significantly weaker than that of non-PVs. This study demonstrated the specific characteristics of the placental endogenous endothelial PGI2 system and the patterns of placental vascular physiological/pharmacological response to exogenous PGI2, showing that placental endothelial PGI2 does not markedly contribute to vascular dilation in the human placenta, in notable contrast to non-PVs. The results provide crucial information for understanding the endothelial roles of HPVs, which may be helpful for further investigations of potential targets in the treatment of diseases such as preeclampsia.