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Bo Zhu, Yumei Chen, Fang Xu, Xiaolu Shen, Xuanyu Chen, Jieqiang Lv, and Songying Zhang

induces the expression of pro-fibrotic growth factors, such as transforming growth factor (TGF-β), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF), during ovarian fibrosis ( 18 ). Pancreatic β cells have a large amount of ER

Open access

Tingting Shu, Zhigang Lv, Yuchun Xie, Junming Tang, and Xuhua Mao

existed in insulin-secreting β-cells ( 3 ), and then other studies showed low concentration of glucose could stimulate hepcidin secretion in pancreatic beta cell line ( 4 , 5 ). Subsequently, the correlation between hepcidin and type 2 diabetes (T2DM) has

Open access

Caio Jordão Teixeira, Junia Carolina Santos-Silva, Dailson Nogueira de Souza, Alex Rafacho, Gabriel Forato Anhe, and Silvana Bordin

). Undisturbed pregnancies in humans and rodents are also distinguished by morphological changes in the pancreatic islets. The most evident morphological adaptations described in the human endocrine pancreas are an increase in the pancreatic β-cell fractional

Open access

Monia Cito, Silvia Pellegrini, Lorenzo Piemonti, and Valeria Sordi

Introduction Type 1 diabetes (T1D) is an autoimmune disorder characterized by insulin-producing β cell death caused by autoreactive T cells ( 1 ). T1D contributes to 10% of the total 422 million diabetes cases worldwide. Although T1D is no

Open access

Li Li, Qifa Song, and Xi Yang

exhaustion of pancreatic β-cells ( 1 ). This deficiency in insulin function is the primary cause for developing a metabolically unhealthy status in patients with obesity who usually display impaired glucose tolerance (IGT) and even type 2 diabetic mellitus (T

Open access

Giorgio Bedogni, Andrea Mari, Alessandra De Col, Sofia Tamini, Amalia Gastaldelli, and Alessandro Sartorio

Introduction The prevalence of childhood type 2 diabetes mellitus (T2DM) is rapidly increasing worldwide ( 1 ). T2DM is characterized by visceral obesity, insulin resistance and defective β-cell function. In children and adolescents, glucose

Open access

Melony C Fortuin-de Smidt, Amy E Mendham, Jon Hauksson, Ali Alhamud, Darko Stefanovski, Olah Hakim, Jeroen Swart, Louise M Goff, Steven E. Kahn, Tommy Olsson, and Julia H Goedecke

The role of ectopic fat, insulin secretion and clearance in the preservation of β-cell function in black African women with obesity who typically present with hyperinsulinemia is not clear. We aim to examine the associations between disposition index (DI, an estimate of β-cell function), insulin secretion and clearance and ectopic fat deposition. This is a cross-sectional study of 43 black South African women (age 20-35 years) with obesity (BMI 30-40 kg/m2) and without type 2 diabetes that measured the following: DI, insulin sensitivity (SI), acute insulin response (AIRg), insulin secretion rate (ISR), hepatic insulin extraction and peripheral insulin clearance (frequently-sampled intravenous glucose tolerance test); pancreatic and hepatic fat, visceral adipose tissue (VAT) and abdominal subcutaneous adipose tissue (aSAT) volume (magnetic resonance imaging), intramyocellular (IMCL) and extramyocellular fat content (EMCL) (magnetic resonance spectroscopy). DI correlated positively with peripheral insulin clearance (β 55.80, p=0.002). Higher DI was associated with lower VAT, pancreatic fat and soleus fat, but VAT explained most of the variance in DI (32%). Additionally, higher first phase ISR (p=0.033) and lower hepatic insulin extraction (p=0.022) associated with lower VAT, independent from SI, rather than with ectopic fat. In conclusion, peripheral insulin clearance emerged as an important correlate of DI. However, VAT was the main determinant of a lower DI above ectopic fat depots. Importantly, VAT, but not ectopic fat, associated with both lower insulin secretion and higher hepatic insulin extraction. Prevention of VAT accumulation in young black African women should therefore be an important target for beta cell preservation.

Open access

Stavroula A Paschou, Nektaria Papadopoulou-Marketou, George P Chrousos, and Christina Kanaka-Gantenbein

Introduction Type 1 diabetes mellitus (T1DM) represents only around 10% of the diabetes cases worldwide, but occurs with increasing incidence much earlier in life. T1DM results from the autoimmune destruction of β cells of the endocrine

Open access

Chenghao Piao, Xiaojie Wang, Shiqiao Peng, Xinyu Guo, Hui Zhao, Li He, Yan Zeng, Fan Zhang, Kewen Zhu, and Yiwei Wang

foetus for development ( 5 ). The need for maternal insulin is an elevated result of gestational insulin resistance, which is impacted by attenuated food intake and placental hormone production. Consequently, the sizes of pancreatic β cells are enhanced

Open access

Thozhukat Sathyapalan, Anne-Marie Coady, Eric S Kilpatrick, and Stephen L Atkin

reduction in insulin resistance especially with weight loss in patients with T2DM will result in normalisation of pancreatic β-cell requirement and even reversal of T2DM ( 9 ). Statins have shown to improve certain features of polycystic ovary syndrome