Although the pathogenesis of metabo

Although the pathogenesis of metabolic syndrome is
unclear, abdominal obesity and insulin resistance have
been proposed to be the predominant causative factors.
Studies using computed tomography have suggested the
importance of fat distribution, and especially the contribution
of abdominal obesity, to the progression of metabolic
syndrome [7]. In particular, accumulation of abdominal fat
induces insulin resistance, and compensatory glucose intolerance
and dyslipidemia, more than subcutaneous fat [7–9].
Additionally, abdominal obesity and insulin resistance are
related to the development of hypertension, type 2 diabetes
and non-alcoholic fatty liver diseases (NAFLD) [7–11].
Recent advances in molecular and cell biology have
shown that adipose tissue stores excess energy in the form
of fat and has important roles in regulating lipid and glucose
homeostasis by secreting physiologically active substances
called adipocytokines [7]. For instance, the obesity gene product leptin, secreted in excess from the enlarged
adipose tissues in obesity, acts as a signal to the central nervous
system indicating the size of energy stores [12].
Adiponectin is one of the most abundant adipose-specific
secretory proteins in rodents and humans [13,14].
The expression of adiponectin is reduced in obesity and
blood levels are negatively correlated with abdominal fat
accumulation [15–18]. Human subjects in hypoadionectinemia,
caused by gene mutation of adiponectin, exhibit dyslipidemia
and impaired glucose tolerance [19,20].
Adiponectin-null mice showed delayed clearance of nonesterified
fatty acids in plasma and severe diet-induced
insulin resistance [21]. Several reports have indicated that
adiponectin can lead to enhanced insulin action in vitro
and in vivo by activating insulin-receptor substrate 1-associated
phosphatidylinositol-3-kinase, AMP-activated protein
kinase and peroxisome proliferator-activated receptor
alpha (PPARa) in liver and muscle [13,21–23], which suggests
strongly that adiponectin has a protective role against
insulin resistance. Over-expression of recombinant adiponectin
had an antiatherogenic effect in apoE-null mice, in
which plaque formation was inhibited significantly compared
with control apoE-null mice [24,25]. Additionally,
clinical and studies in vitro have indicated that levels of
plasma adiponectin are positively correlated with levels of
plasma HDL-cholesterol in humans [18,26] and adiponectin
increased HDL assembly in human hepatocytes [27].
These results suggest that adiponectin reveals antiatherogenic
action by accelerating the whole-body reverse cholesterol
transport system. It has been reported that the
concentration of plasma adiponectin in patients with
hypertension was significantly lower than in normotensive
healthy subjects [28–30], and adiponectin-null mice showed
hypertension compared with wild-type mice [31]. These
results suggest that plasma adiponectin is an independent
regulatory factor for blood pressure.

Results (Indonesian) 2:

Meskipun patogenesis sindrom metabolik adalah
jelas, obesitas abdominal dan resistensi insulin telah
diusulkan untuk menjadi faktor penyebab dominan.
Studi menggunakan computed tomography telah menyarankan
pentingnya distribusi lemak, dan terutama kontribusi
dari obesitas perut, untuk perkembangan metabolik
sindrom [7]. Secara khusus, penumpukan lemak perut
menginduksi resistensi insulin, dan intoleransi glukosa kompensasi
dan dislipidemia, lebih dari subkutan lemak [7-9].
Selain itu, obesitas abdominal dan resistensi insulin yang
terkait dengan pengembangan hipertensi, diabetes tipe 2
dan non-alkohol penyakit fatty liver (NAFLD) [11/07].
kemajuan terbaru dalam biologi molekuler dan seluler telah
menunjukkan bahwa toko jaringan adiposa kelebihan energi dalam bentuk
lemak dan memiliki peran penting dalam mengatur lipid dan glukosa
homeostasis dengan mengeluarkan zat aktif fisiologis
disebut adipocytokines [ 7]. Misalnya, leptin obesitas produk gen, disekresikan lebih dari pembesaran
jaringan adiposa pada obesitas, bertindak sebagai sinyal ke saraf pusat
sistem yang menunjukkan ukuran toko energi [12].
Adiponektin merupakan salah satu yang paling berlimpah adiposa khusus
sekretorik protein pada hewan pengerat dan manusia [13,14].
ekspresi adiponektin berkurang pada obesitas dan
kadar darah berkorelasi negatif dengan lemak perut
akumulasi [15-18]. Subyek manusia di hypoadionectinemia,
disebabkan oleh mutasi gen adiponektin, pameran dislipidemia
dan gangguan toleransi glukosa [19,20].
Tikus Adiponektin-nol menunjukkan tertunda clearance nonesterified
asam lemak dalam plasma dan diet-induced parah
resistensi insulin [21]. Beberapa laporan telah menunjukkan bahwa
adiponektin dapat mengarah pada tindakan insulin ditingkatkan in vitro
dan in vivo dengan mengaktifkan reseptor insulin substrat 1-terkait
phosphatidylinositol-3-kinase, AMP-activated protein
kinase dan Peroksisom proliferator-activated receptor
alpha (PPARa) di hati dan otot [13,21-23], yang menunjukkan
sangat adiponektin yang memiliki peran protektif terhadap
resistensi insulin. Over-ekspresi adiponektin rekombinan
memiliki efek antiatherogenic pada tikus apoE-nol, di
mana pembentukan plak dihambat secara signifikan dibandingkan
dengan kontrol tikus apoE-nol [24,25]. Selain itu,
klinis dan studi in vitro telah menunjukkan bahwa tingkat
adiponektin plasma berkorelasi positif dengan tingkat
plasma HDL-kolesterol pada manusia [18,26] dan adiponektin
meningkat perakitan HDL dalam hepatosit manusia [27].
Hasil ini menunjukkan bahwa adiponektin mengungkapkan antiatherogenic
tindakan dengan mempercepat seluruh tubuh membalikkan kolesterol
sistem transportasi. Telah dilaporkan bahwa
konsentrasi adiponektin plasma pada pasien dengan
hipertensi secara signifikan lebih rendah daripada di normotensive
subyek sehat [28-30], dan tikus adiponektin-nol menunjukkan
hipertensi dibandingkan dengan jenis tikus liar [31]. Ini
hasil menunjukkan bahwa adiponektin plasma adalah independen
faktor regulasi tekanan darah.