SavedAdd your journal

Journals / Turkish Journal of Gastroenterology / 2016 / Cilt: 27 - Sayı: 1

Ovaries are more vulnerable than hepatocytes for insulin resistance and hyperinsulinemia

İLHAMİ GÜLTEPE
Metin BAŞARANOĞLU
Yaser SÜLEYMANOĞLU
Gökçen BAŞARANOĞLU
Fatma BEYAZIT
Pages
62–67
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: This study showed that rather than pancreatic beta-cell hyperfunction, insulin resistance plays a central role in the development of ovarian abnormalities

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/Aims: Non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) are common metabolic disorders.
📊
Key Findings & Data:Materials and Methods: Thirty female patients with NAFLD and without PCOS; 12 female patients with PCOS; and a control group with 17 healthy females were included.
💡
Conclusion & Impact:Conclusion: This study showed that rather than pancreatic beta-cell hyperfunction, insulin resistance plays a central role in the development of ovarian abnormalities
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Background/Aims: Non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) are common metabolic disorders. We aimed to evaluate the underlying mechanisms in the development of NAFLD and PCOS. Materials and Methods: Thirty female patients with NAFLD and without PCOS; 12 female patients with PCOS; and a control group with 17 healthy females were included. Pancreatic homeostatic model assessment-Beta cell function was measured by the homeostasis model assessment (HOMA)-B test.Results: The body mass index (BMI) of the NAFLD patients was higher than that of the PCOS patients (29.4±3.8 kg/m² vs 25.6±5.2 kg/m², p<0.05). There was no significant difference between the PCOS patients and controls with respect to BMI. The fasting insulin levels of the NAFLD patients were higher than those of the PCOS patients (5.06 unit more than PCOS, p<0.05) and 12.8 unit more than controls (p<0.001). The HOMA scores of the NAFLD patients were more than those of the PCOS patients (1.41 unit more than PCOS, p<0.05) and 2.95 unit more than controls (p<0.001). The HOMA-B score was higher in the NAFLD patients than in the PCOS patients. There was no statistical difference among the groups for serum triglyceride (p>.05) and cholesterol (p>.05). Conclusion: This study showed that rather than pancreatic beta-cell hyperfunction, insulin resistance plays a central role in the development of ovarian abnormalities

🔖

Cite This Article

GÜLTEPE, İ., BAŞARANOĞLU, M., SÜLEYMANOĞLU, Y., BAŞARANOĞLU, G., BEYAZIT, F. (2016). Ovaries are more vulnerable than hepatocytes for insulin resistance and hyperinsulinemia. Turkish Journal of Gastroenterology, Cilt: 27 - Sayı: 1, 62–67. https://ajindex.com/articles/410743

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Younossi ZM, Diehl AM, Ong JP. Nonalcoholic fatty liver disease: an agenda for clinical research. Hepatology 2002; 35: 746-52.
  2. Basaranoglu M, Basaranoglu G, Sabuncu T, Sentürk H. Fructose as a key player in the development of fatty liver disease. World J Gastroenterol 2013; 19: 1166-72.
  3. Garcia-Monzon C, Martin-Perez E, Iacono OL, et al. Characteriza- tion of pathogenic and prognostic factors of nonalcoholic steato- hepatitis associated with obesity. J Hepatol 2000; 33: 716-24.
  4. Sonsuz A, Basaranoglu M, Bilir M, et al. Hyperinsulinemia in non- diabetic, both obese and nonobese patients with nonalcoholic steatohepatitis. Am J Gastroenterol 2002; 97: 495. Basaranoglu M, Sonsuz A, Senturk H, Akin P. The low incidence of primary liver disease in patients with nonalcoholic steatohepati- tis. J Hepatol 2001; 35: 684-5.
  5. Baffy G, Brunt EM, Caldwell SH. Hepatocellular carcinoma in non- alcoholic fatty liver disease: an emerging menace. J Hepatol 2012; 56: 1384-91. Sanyal AJ. Insulin resistance and nonalcoholic steatohepatitis: fat or fiction? Am J Gastroenterol 2001; 96: 274-6.
  6. Sanyal AJ, Campbell-Sargent C, Mirshahi F, et al. Nonalcoholic ste- atohepatitis: association of insulin resistance and mitochondrial abnormalities. Gastroenterology 2001;120: 1183-92
  7. Kayaçetin S, Başaranoğlu M. Mallory-Denk bodies: Correlation with steatosis, severity, zonal distribution, and identification with ubiquitin. Turk J Gastroenterol 2015; 26: 506-10. Taketani Y. Pathophysiology of polycystic ovary syndrome. Horm Res 1990; 33: 3-4. Lobo RA. Hirsutism in polycystic ovary syndrome: current con- cepts. Clin Obst Gynecol 1991; 34: 817-26.
  8. Acien P, Quereda F, Matall P, et al. Insulin, androgens, and obesity in women with and without polycystic ovary syndrome; a heter- ogenous group of disorders. Fertil Steril 1999; 72:32-40.
  9. Laboureau-Soares Barbosa S, Rodien P, Rohmer V. Polycystic ovary syndrome: treatment with insulin-sensitizing agents. Ann Endo- crinol 2002; 63: 31-5.
  10. Fulghesu AM, Ciampelli M, Muzj G, et al. N-acetyl-cysteine treat- ment improves insulin sensitivity in women with polycystic ovary syndrome. Fertil Steril 2002; 77: 1128-35.
  11. Caldwell SH, Hespenheide EE, Redick JA, et al. A pilot study of a thiazolidinedione, troglitazone, in nonalcoholic steatohepatitis. Am J Gastroenterol 2001; 96: 519-25.
  12. Youssef W, McCullough AJ. Diabetes mellitus, obesity, and he- patic steatosis. Semin Gastrointest Dis 2002; 13: 17-30. National Research Council. Diet and Health: Implications for R