Intervensi Nikotin Terhadap Profil Lipid Ekspresi UCP-1 (Uncoupling Protein-1) Pada Monyet Ekor Panjang (Macaca fascicularis)Obes dengan Risiko Aterogenik

Abstract

Pola makan dengan tinggi kalori tanpa disertai dengan pengaturan keseimbangan energi antarakalori yang dikonsumsi dan kalori yang dikeluarkan merupakan penyebab dasarkelebihan berat badan yang mengarah ke obesitas. Kondisi ini sudah menjadi masalah global terutama di negara-negara berkembang dan di negara-negara maju olehkarena memiliki berbagai faktor resiko terhadap sindrom metabolik yang berkaitan dengan penyakit jantung koroner (PJK), diabetes melitus, dan hipertensi. Kelebihan berat badan pada sindrom metabolik dengan resiko tinggi aterosklerosis (atherogenetic process) diidentifikasi melalui adanya peningkatan indeks bobot badan (body mass index; BMI), lingkar pinggang atau rasio lingkar pinggang dan pinggul. Jaringan adipos dikenal sebagai tempat penyimpanan triglserida (TG), dan sebagai jaringan endokrin dinamik yang mengsekresikan free fatty acid (FAA) dan berbagai protein seperti adiponectin dan adipokin. Adapun profi lipid yang penting untuk mendiagnosis hiperlipoproteinemia yang mencakup ~lipidemia meliputi peubah kolesterol totai trigliserida, LDL-kolesterol dan HDL-kolesterol. Jaringan adipose diketahui pula sebagai organ endokrinaktif yang dapat mengsekresikan berbagai adipokin dan salah satunya adiponektin berperan dalam metabolisme lipid dan karbohidrat dalam sirkulasi darah dan berpotensi dalam sindrom metabolik.

Obesityis an abnormal accumulation of body fat with increased risk of coroner heart disease atherosclerosis, indicated by hyperlipoproteinemia. There are many treatments to prevent metabolic syndrome related to obesity, particularly with atherosclerosis risk. The aims of this study were to obtain information of metabolic changes through lipid profile and body weight also to evaluate UCP-1 expression post nicotine intervention on cynomolgus monkey with atherogenic risk. Fifteen animals were divided into three groups, given isocaloric diets containing 1) beef tallow (as diet A); 2) beeftallow and egg yolk (as Diet B) and other primary materials, and 3) commercial monkey chow diet (as a control or as Diet C). These diets were given for one year to develop obesity, then continued for three months by additing nicotine in their diet at a dose of at least 0. 75 mg I kg body weight every 12 hours. Body weight and lipid profile were analyzed every months and brown adipose tissue was taken at necropsy for evaluating UCP-1 expression by using antibody fluoresence technique. This study used a complete randomized design (ANOV A) to analyzes body weight and lipid profile. There were significantly increased in total plasma cholesterolconcentration (p<0.01), especially for diet type B and triglyceride concentration was not significantly increased (p>0.01). Followed by significantly increased HDL and LDL level, however there was decreased in body weight. Evaluation of UCP expression in this study showed expression of UCP-1 in each diet group A, B and C. Group B showed to have higher expression of UCP-1 than the other groups.