ارتباط بیان ژنی ACE و GHRL با بیماری مزمن کبد چرب: بینش‌های بالینی و متابولیک

نوع مقاله : مقاله پژوهشی

نویسنده

گروه شیمی و بیوشیمی، دانشکده پزشکی، دانشگاه بابل، عراق

چکیده

هدف: بیماری کبد چرب (FLD) یا استئاتوز کبدی، یک وضعیت پاتولوژیک است که با تجمع بیش از حد چربی در کبد بیش از ۵ تا ۱۰ درصد وزن آن تعریف می‌شود. با توجه به علل چندعاملی این بیماری که شامل اختلالات متابولیک و زمینه‌های ژنتیکی است، این پژوهش با هدف بررسی ارتباط میان شاخص‌های بیوشیمیایی، بیان ژنی ACE و GHRL و متغیرهای جمعیت‌شناختی مانند سن و شاخص توده بدنی (BMI) در بیماران مبتلا به FLD در مقایسه با افراد سالم انجام شد.
مواد و روش‌ها: در این مطالعه ۲۰۰ نفر شرکت کردند که شامل ۱۰۰ بیمار مبتلا به FLD تأیید شده با سونوگرافی (G2) و ۱۰۰ فرد سالم همسان از نظر سن و قومیت (عراقی) به عنوان گروه کنترل (G1) بودند. تمامی افراد بزرگسال غیرسیگاری با محدوده سنی ۲۰ تا ۶۰ سال بودند که از بیمارستان آموزشی دیوانیه، عراق انتخاب شدند. آزمایش‌های بیوشیمیایی استاندارد برای اندازه‌گیری کراتینین، اوره خون، انسولین، قند خون ناشتا (FBS)، هموگلوبین گلیکوزیله (HbA1c)، کلسترول تام (TC)، تری‌گلیسرید (TG)، لیپوپروتئین با چگالی بالا (HDL)، لیپوپروتئین با چگالی بسیار پایین (VLDL)، آلانین آمینوترانسفراز (ALT)، آسپارتات آمینوترانسفراز (AST)، نسبت AST/ALT و آلکالین فسفاتاز (ALP) انجام شد. هم‌زمان، تحلیل کمی بیان ژن ACE و GHRL صورت گرفت و سطوح بیان برای ارتباط بالینی با اختلالات متابولیک در FLD بررسی شد.
نتایج: بیماران مبتلا به FLD در مقایسه با گروه کنترل دارای مقادیر بالاتر معنی‌دار در شاخص توده بدنی، کراتینین، اوره خون، انسولین، FBS، HbA1c، TC، TG، VLDL، ALT، AST و ALP بودند، در حالی که سطح HDL به‌طور معناداری پایین‌تر بود (P < 0.05). به‌طور مهم، سطح بیان ژن‌های ACE و GHRL در گروه FLD افزایش قابل توجهی داشت که با ناهنجاری‌های بیوشیمیایی مشاهده‌شده همبستگی نشان داد. این نتایج تعامل میان تغییرات بیان ژن و اختلالات متابولیک در پاتوفیزیولوژی FLD را تقویت می‌کند.
نتیجه‌گیری: مقادیر P به‌طور مداوم کمتر از 05/0، استحکام ارتباطات مشاهده‌شده را تأیید می‌کند. تغییر در بیان ژن‌های ACE و GHRL می‌تواند به عنوان نشانگرهای مولکولی قابل اعتماد برای شناسایی افراد در معرض خطر بالاتر پیشرفت FLD به‌کار رود. افزون بر این، ارزیابی گسترده شاخص توده بدنی، شاخص‌های عملکرد کلیوی، شاخص‌های گلیسمی، پروفایل‌های چربی و فعالیت آنزیم‌های کبدی، بینش ارزشمند بالینی فراهم کرده و از رویکرد یکپارچه برای تشخیص زودهنگام و مدیریت FLD پشتیبانی می‌کند.

کلیدواژه‌ها


عنوان مقاله [English]

Association of genetic expression of the ACE and GHRL genes with chronic fatty liver disease: clinical and metabolic insights

نویسنده [English]

  • Tariq Hussein Mgheer
Department of Chemistry and Biochemistry, College of Medicine, University of Babylon, Iraq.
چکیده [English]

Objective
Fatty liver disease (FLD), or hepatic steatosis, is a pathological condition described by excessive lipid accumulation surpassing 5–10% of liver weight. Given its multifactorial etiology, involving both metabolic dysfunction and genetic predisposition, this investigation aimed to investigate the relationship between biochemical parameters, expression of the ACE and GHRL genes, and demographic variables like age and body mass index (BMI) in patients with FLD compared with healthy controls.
Materials and methods
The investigation enrolled 200 individuals, comprising 100 patients with ultrasonographically affirmed FLD (G2) and 100 age- and ethnicity-matched healthy controls of Iraqi descent (G1). All participants were non-smoking adults between 20 and 60 years recruited from Diwaniyah Teaching Hospital, Iraq. Standardized biochemical assays were carried out to calculate creatinine, blood urea, insulin, fasting blood sugar (FBS), glycated hemoglobin (HbA1c), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), very-low-density lipoprotein (VLDL), alanine aminotransferase (ALT), aspartate aminotransferase (AST), AST/ALT ratio, and alkaline phosphatase (ALP). In parallel, quantitative gene expression analysis of ACE and GHRL was conducted, and expression levels were validated for clinical relevance to metabolic disturbances in FLD.
Results
Patients with FLD showed meaningfully higher BMI, creatinine, blood urea, insulin, FBS, HbA1c, TC, TG, VLDL, ALT, AST, and ALP levels compared to controls, along with markedly lower HDL levels (P < 0.05). Importantly, expression levels of both ACE and GHRL genes were meaningfully upregulated in the FLD group, correlating with the biochemical abnormalities observed. These results reinforce the interaction between altered gene expression and metabolic derangements in FLD pathophysiology.
Conclusion
The consistently low P-values (P < 0.05) affirm the robustness of the associations observed. Altered expression of ACE and GHRL genes may serve as reliable molecular biomarkers for identifying individuals at higher risk of FLD progression. Furthermore, wide evaluation of BMI, renal function markers, glycemic indices, lipid profiles, and liver enzyme activities supplies worth clinical discernment, supporting an integrative approach to early diagnosis and management of FLD.

کلیدواژه‌ها [English]

  • Fatty liver disease
  • hepatic steatosis
  • ACE gene
  • GHRL gene
  • biomarkers
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