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"Tesis ini bertujuan untuk mengetahui korelasi antara ekspresi reseptor leptin endometrium dengan ekspresi reseptor αvβ3 integrin endometrium pada fase luteal madya pasien infertilitas, untuk mencari tahu salah satu penyebab kegagalanimplantasi. Nilai leptin lokal endometrium dinilai melalui ekspresi leptin endometriumdan daya terima endometrium dinilai melalui ekspresi reseptor αvβ3 integrinendometrium. Penelitian ini dengan desain potong lintang di RSUPN Dr. CiptoMangunkusumo. Ekspresi reseptor dinilai dari H-score pada pewarnaanimunohistokimia yang diambil dengan cara biopsi endometrium sebagai baku emas. Dari 30 sampel didapatkan ekspresi reseptor leptin endometrium baik pada 23 sampel (76,7%), ekspresi reseptor leptin endometrium buruk pada 7 sampel (23,3%), sedangkan hasil daya terima endometrium baik pada 24 sampel (80%), dan dayaterima endometrium buruk pada 6 sampel (20%). Uji analisis membuktikkan kadarleptin serum berkorelasi kuat dengan ekspresi leptin endometrium (r=0,67;p<0,01)dengan ekspresi leptin endometrium, dan ekspresi leptin endometrium berkorelasidengan daya terima endometrium (r=0,72;p<0,01). Analisis multivariat menyebutkanfaktor-faktor yang berpengaruh terhadap daya terima endometrium secara berurutanadalah progesteron, ekspresi leptin endometrium, dan kadar leptin serum. ;The aim of this study is to correlate between endometrial leptin receptor expressionwith endometrial integrin αvβ3 expression on mid luteal phase of infertility patients toknow one of the cause of implantation failure. Leptin played important role in femaleneuroendocrine and endometrial implantation. Local leptin value were assessedthrough the expression of leptin endometrial receptor and endometrial receptivityassessed through the expression of integrin αvβ3 endometrial. This study was crosssectionaldesigninRSUPNDr.CiptoMangunkusumo.TheexpressionofthereceptorratedofH-scoreon immunohistochemical staining were taken by endometrial biopsyas the gold standard. From 30 samples obtained, good endometrial leptin receptor expression were found in 23 samples (76.7%), poor endometrial leptin receptorexpression in were found 7 samples (23.3% ), good endometrial receptivity werefound in 24 samples (80%) and poor endometrial receptivity in 6 samples (20%).Result of this study show leptin serum was strongly correlated (r=0,67;p<0,01) withleptin endometrial receptor expression and endometrial leptin receptor expression wasstrongly correlated with endometrial integrin αvβ3 expression (r=0,72;p<0,01).Multivariate analysis show factors that correlate to endometrial receptivitysequentially are progesterone, endometrial leptin receptor, and leptin serum. "

"Salah satu mekanisme terjadinya resistensi leptin pada obesitas adalah kelainan reseptor leptin (Ob-R)."

"Salah satu mekanisme terjadinya resistemi leptin pada obesitas adalah kelainan reseptor leptin (Ob-R). Beberapa penelitian membuklikan bahwa aktifitas ikatan leptin di serum manusia berhubungan dengan reseptor leptin terlarut (soluble leptin receptor) dan restriksi asupan energi menyebabkan penurunan kadar leptin darah. Penelitian ini adalah untuk mengetahui beda kadar reseptor leptin terlarut serum dan densitas reseptor leptin dijaringan lemak adventitial aorta setelah dilakukan restriksi diet selama 4 minggu. Kadar reseptor leptin terlarut diukur dengan ELISA dan densitas reseptor leptin di jaringan lemak dengan irnunohistokimia. Kadar reseptor leptin terlarut pada kelompok perlakuan 40% diet normal lebih rendah dibanding kontrol (p=0,02). Tidak didapaikan perbedaan reseptor leptin terlarut yang bermakna antara kelompok perlakuan 40% diet normal, 1 hari puasa-1 hari makan normal dan 1 hari pitasa-2 hari makan normal. Di sisi lain, densitas reseplor leptin dijaringan lemak advenlitia aorta justru lebih tinggi pada kelompok restriksi 40% daripada kontrol. Restriksi diet 40% kalori normal harian menurunkan kadar reseptor leptin terlarut di serum, tetapi meningkatkan densitas reseptor leptin dijaringan lemak advential aorta tikus. Perubahan ini mungkin merupakan akibat mekanisme up regulation dalani mempertahankan homeostasis. (Med J Indones 2006; 15:145-50)

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One of the five possible mechanisms of leptin resistance in human obesity is the defect in the leptin receptor (Ob-R). Evidence has accumulated that leptin-binding activity in human serum is related to a soluble form of the leptin receptor, and restriction of energy intake resulted a decrease in circulating leptin levels. Aim of this study is to examine the difference of serum soluble leptin receptor level and ieplin receptor density in rat adipose tissue of adventitial aorta after four weeks treated with different restricted diets. Soluble leptin receptor level was measured by ELISA and leptin receptor density by using immuno-hisfochemistry. The soluble leptin receptor in group treated with 40% of normal daily calori diet was found significantly lower than control (p = 0.02). There were no any significant differences among group treated with 40 % of normal daily calori diet, "I day fast-] day eat", and "ldayfaxt-2 days eat" groups, and among I day fast-1 day eat", "day fast - 2 days eat" and control groups as well. On the other hand, leptin receptor density in adipose tissues was higher in restricted diet group than control. Diet of 40 % normal daily calorie for 4 weeks decreased soluble leptin receptor level, but increased adipocyte leptin receptor density of the adipose tissue of rat adventitial aorta. These changes may be resulted from an up regulation mechanism in relation with homeostatic maintenance. (Med J Indones 2006; 15:145-50)"

"Sindrom ovarium polikistik (SOPK) diketahui terkait dengan obesitas melalui: resistensi leptin. Salah satu penyebab resistensi leptin adalah defisiensi reseptor leptin (LEPR) dibubarkan. Tujuan dari penelitian ini adalah untuk menentukan ekspresi mRNA dari LEPR. gen dilarutkan pada subjek obesitas dan non-obesitas dengan PCOS dan non-SOPK sertamengetahui korelasi antara ekspresi gen tersebut dengan obesitas dan PCOS. Kecepatan Ekspresi mRNA gen LEPR dalam sampel darah diukur menggunakan metode waktu nyata PCR. Penelitian dilakukan pada 96 subjek dengan empat kelompok sampel, yaitu: PCOS non-obesitas, PCOS bebas obesitas, PCOS obesitas, dan PCOS obesitas. Hasil pengukuran menunjukkan ekspresi mRNA rata-rata dari gen LEPR terlarut di masing-masing kelompok 2,10 x 10-4 ng/μL ± 1,88 x 10-4; 1,27 x 10-4 ng/μL ± 1,31 x 10-4; 1,99x 10-4 ng/μL ± 2,35 x 10-4; dan 1,44 x 10-4 ± 2,21 x 10-4 ng/μL. LEPR. ekspresi gen mRNA terlarut dalam semua kelompok obesitas diketahui lebih rendah jika dibandingkan dengankelompok obesitas (P < 0,05) dan tidak ada perbedaan yang signifikan antara kelompok umum tanpa PCOS dan PCOS (1,69 x 10-4 ± 1,65 x 10-4; 1,71 x 10-4 ± 2,27 x 10- 4, P > 0,05). Studi ini menemukan bahwa penurunan ekspresi mRNA dari gen LEPR yang larut berhubungan dengan obesitas dan tidak berhubungan dengan PCOS.Polycystic ovary syndrome (SOPK) is known to be associated with obesity through: leptin resistance. One of the causes of leptin resistance is dissolved leptin receptor (LEPR) deficiency. The aim of this study was to determine the mRNA expression of LEPR. gene was dissolved in obese and non-obese subjects with PCOS and non-PCOS as well asdetermine the correlation between the expression of these genes with obesity and PCOS. Expression velocity of LEPR gene mRNA in blood samples was measured using real-time PCR method. The study was conducted on 96 subjects with four sample groups, namely: non-obese PCOS, obesity-free PCOS, obese PCOS, and obese PCOS. The measurement results showed the average mRNA expression of the soluble LEPR gene in each group was 2.10 x 10-4 ng/μL ± 1.88 x 10-4; 1.27 x 10-4 ng/μL ± 1.31 x 10-4; 1.99x 10-4 ng/μL ± 2.35 x 10-4; and 1.44 x 10-4 ± 2.21 x 10-4 ng/μL. LEPR. soluble mRNA gene expression in all obesity groups was found to be lower when compared to obese group (P < 0.05) and there was no significant difference between the general group without PCOS and PCOS (1.69 x 10-4 ± 1.65 x 10-4; 1.71 x 10-4 ± 2.27 x 10-4, P > 0.05). This study found that decreased mRNA expression of the soluble LEPR gene was associated with obesity and not associated with PCOS."