tion in insulin signaling pathways

tion in insulin signaling pathways [1,2], such that a decrease in body zinc status might cause insulin resistance [33,34]. The issue of whether serum zinc levels are associated with
plasma lipids is controversial. In agreement with our results, Ghasemi et al. [18] found a positive correlation between serum zinc levels and triglycerides in Iranian men whereas no association was observed between serum zinc concentrations and lipid profiles in a Kuwaiti population [37] or in Lebanese adults [38]. Although several studies have shown no association between serum zinc levels and HDL-cholesterol concentrations [18,37,38], we found a trend for a negative association between serum zinc and HDLcholesterol levels in both men and women. Additionally, in a metaanalysis of 33 randomized controlled trials, no significant effects of
zinc supplementation on serum lipids were observed, but zinc supplementation was associated with a significant decrease in HDL-cholesterol levels in a sub-group analysis of healthy participants, and HDL-cholesterol levels increased as a result of zinc supplementation in a sub-group analysis of subjects with type 2 diabetes mellitus [39]. However, the negative association
between serum zinc and lipoprotein metabolism in our study should be considered cautiously, including the influence of zincrich foods such as red meat on plasma lipids [40] and various health conditions known to influence zinc homeostasis [41–44], and further investigations considering these factors are warranted to confirm the association between serum zinc levels and lipid profiles. Other factors not included in the clinical definition of MetS, such as chronic inflammation [16] or oxidative stress [15], may lead to the development of MetS. Inflammatory cytokines released by visceral fat [45], including tumor necrosis factor-a(TNF-a), interleukin-6 (IL-6) and plasminogen activator inhibitor-1 (PAI-1), stimulate C-reactive protein (CRP) production in the liver, and these processes are associated with MetS [17]. On the other hand,
oxidative stress, which occurs when reactive oxygen species (ROS) exceed the antioxidant capacity, may play an important role in MetS [15]. Zinc reduces inflammatory cytokine production via upregulation of a zinc-finger protein, which inhibits nuclear factorkB (NF-kB) activation [6,7]. Furthermore, zinc, a cofactor for antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase, decreases ROS generation and induces metallothionein, which decreases the OH burden [2], suggesting that a decrease in body zinc status may contribute to the development or aggravation of MetS. In addition, chronic inflammation or oxidative stress may contribute to the decreased serum zinc levels.

Hasil (Bahasa Indonesia) 2:

tion insulin jalur sinyal [1,2], sehingga penurunan status seng tubuh dapat menyebabkan resistensi insulin [33,34]. Masalah apakah kadar serum seng berhubungan dengan
lipid plasma kontroversial. Dalam perjanjian dengan hasil kami, Ghasemi et al. [18] menemukan korelasi positif antara kadar zinc serum dan trigliserida pada pria Iran namun hubungan yang diamati antara konsentrasi zinc serum dan profil lipid pada populasi Kuwait [37] atau pada orang dewasa Lebanon [38]. Walaupun beberapa penelitian telah menunjukkan tidak ada hubungan antara kadar zinc serum dan konsentrasi HDL-kolesterol [18,37,38], kami menemukan kecenderungan untuk hubungan negatif antara seng serum dan kadar HDLcholesterol baik pada pria maupun wanita. Selain itu, dalam metaanalisis dari 33 percobaan acak terkontrol, tidak ada efek signifikan
suplementasi zinc pada lipid serum yang diamati, tapi suplemen seng dikaitkan dengan penurunan yang signifikan dalam kadar HDL-kolesterol dalam analisis sub-kelompok peserta yang sehat, dan HDL kadar kolesterol meningkat sebagai akibat dari suplemen zinc dalam analisis sub-kelompok subjek dengan diabetes mellitus tipe 2 [39]. Namun, asosiasi negatif
antara seng serum dan metabolisme lipoprotein dalam penelitian kami harus dipertimbangkan dengan hati-hati, termasuk pengaruh dari makanan zincrich seperti daging merah pada lipid plasma [40] dan berbagai kondisi kesehatan diketahui mempengaruhi homeostasis seng [41-44], dan penyelidikan lebih lanjut mempertimbangkan faktor-faktor ini dijamin untuk mengkonfirmasi hubungan antara kadar seng serum dan profil lipid. Faktor-faktor lain yang tidak termasuk dalam definisi klinis Mets, seperti peradangan kronis [16] atau stres oksidatif [15], dapat menyebabkan perkembangan Mets. Sitokin inflamasi dirilis oleh lemak visceral [45], termasuk tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6) dan plasminogen activator inhibitor-1 (PAI-1), merangsang C-reactive protein (CRP) produksi di hati, dan proses ini terkait dengan Mets [17]. Di sisi lain,
stres oksidatif, yang terjadi ketika spesies oksigen reaktif (ROS) melebihi kapasitas antioksidan, dapat memainkan peran penting dalam Mets [15]. Zinc mengurangi produksi sitokin inflamasi melalui peningkatan regulasi protein seng-jari, yang menghambat factorkB nuklir (NF-kB) aktivasi [6,7]. Selain itu, seng, kofaktor untuk enzim antioksidan, seperti superoksida dismutase dan glutation peroksidase, menurunkan generasi ROS dan menginduksi metallothionein, yang menurunkan beban OH [2], menunjukkan bahwa penurunan status zinc tubuh dapat berkontribusi untuk pengembangan atau kejengkelan Mets. Selain itu, kronis peradangan atau oksidatif stres dapat berkontribusi untuk kadar zinc serum menurun.