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Original Article
Obesity and Metabolic Syndrome
In Vitro Effect of Fatty Acids Identified in the Plasma of Obese Adolescents on the Function of Pancreatic β-Cells
Claudia Velasquez, Juan Sebastian Vasquez, Norman Balcazar
Diabetes Metab J. 2017;41(4):303-315.   Published online May 24, 2017
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  • 8 Web of Science
  • 6 Crossref
AbstractAbstract PDFPubReader   

The increase in circulating free fatty acid (FFA) levels is a major factor that induces malfunction in pancreatic β-cells. We evaluated the effect of FFAs reconstituted according to the profile of circulating fatty acids found in obese adolescents on the viability and function of the murine insulinoma cell line (mouse insulinoma [MIN6]).


From fatty acids obtained commercially, plasma-FFA profiles of three different youth populations were reconstituted: obese with metabolic syndrome; obese without metabolic syndrome; and normal weight without metabolic syndrome. MIN6 cells were treated for 24 or 48 hours with the three FFA profiles, and glucose-stimulated insulin secretion, cell viability, mitochondrial function and antioxidant activity were evaluated.


The high FFA content and high polyunsaturated ω6/ω3 ratio, present in plasma of obese adolescents with metabolic syndrome had a toxic effect on MIN6 cell viability and function, increasing oxidative stress and decreasing glucose-dependent insulin secretion.


These results could help to guide nutritional management of obese young individuals, encouraging the increase of ω-3-rich food consumption in order to reduce the likelihood of deterioration of β-cells and the possible development of type 2 diabetes mellitus.


Citations to this article as recorded by  
  • The reversible effects of free fatty acids on sulfonylurea-stimulated insulin secretion are related to the expression and dynamin-mediated endocytosis of KATP channels in pancreatic β cells
    Chenmin Wei, Zichen Zhang, Qi Fu, Yunqiang He, Tao Yang, Min Sun
    Endocrine Connections.2023;[Epub]     CrossRef
  • Preparation of fatty acid solutions exerts significant impact on experimental outcomes in cell culture models of lipotoxicity
    Axel Römer, Divya Rawat, Thomas Linn, Sebastian F Petry
    Biology Methods and Protocols.2022;[Epub]     CrossRef
  • Lipotoxic Impairment of Mitochondrial Function in β-Cells: A Review
    Axel Römer, Thomas Linn, Sebastian F. Petry
    Antioxidants.2021; 10(2): 293.     CrossRef
  • Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic β-Cells to Type 2 Diabetes
    Petr Ježek, Martin Jabůrek, Lydie Plecitá-Hlavatá
    Antioxidants & Redox Signaling.2019; 31(10): 722.     CrossRef
  • The role of polyunsaturated fatty acids (n-3 PUFAs) on the pancreatic β-cells and insulin action
    Habtamu Wondifraw Baynes, Seifu Mideksa, Sintayehu Ambachew
    Adipocyte.2018; : 1.     CrossRef
  • Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity
    Petr Ježek, Martin Jabůrek, Blanka Holendová, Lydie Plecitá-Hlavatá
    Molecules.2018; 23(6): 1483.     CrossRef
Novel Molecular Mechanisms in the Development of Non-Alcoholic Steatohepatitis
Davide Povero, Ariel E. Feldstein
Diabetes Metab J. 2016;40(1):1-11.   Published online February 19, 2016
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  • 55 Download
  • 45 Web of Science
  • 46 Crossref
AbstractAbstract PDFPubReader   

Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in adults and children worldwide. NAFLD has become a severe health issue and it can progress towards a more severe form of the disease, the non-alcoholic steatohepatitis (NASH). A combination of environmental factors, host genetics, and gut microbiota leads to excessive accumulation of lipids in the liver (steatosis), which may result in lipotoxicity and trigger hepatocyte cell death, liver inflammation, fibrosis, and pathological angiogenesis. NASH can further progress towards liver cirrhosis and cancer. Over the last few years, cell-derived extracellular vesicles (EVs) have been identified as effective cell-to-cell messengers that transfer several bioactive molecules in target cells, modulating the pathogenesis and progression of NASH. In this review, we focused on recently highlighted aspects of molecular pathogenesis of NASH, mediated by EVs via their bioactive components. The studies included in this review summarize the state of art regarding the role of EVs during the progression of NASH and bring novel insight about the potential use of EVs for diagnosis and therapeutic strategies for patients with this disease.


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Glucolipotoxicity in Pancreatic β-Cells
Ji-Won Kim, Kun-Ho Yoon
Diabetes Metab J. 2011;35(5):444-450.   Published online October 31, 2011
  • 54,718 View
  • 101 Download
  • 59 Crossref
AbstractAbstract PDFPubReader   

The recent epidemic of type 2 diabetes in Asia differs from that reported in other regions of the world in several key areas: it has evolved over a much shorter time, in an earlier stage of life, and in people with lower body mass indices. These phenotypic characteristics of patients strongly suggest that insulin secretory defects may perform a more important function in the development and progression of diabetes. A genetic element clearly underlies β-cell dysfunction and insufficient β-cell mass; however, a number of modifiable factors are also linked to β-cell deterioration, most notably chronic hyperglycemia and elevated free fatty acid (FFA) levels. Neither glucose nor FFAs alone cause clinically meaningful β-cell toxicity, especially in patients with normal or impaired glucose tolerance. Thus the term "glucolipotoxicity" is perhaps more appropriate in describing the phenomenon. Several mechanisms have been proposed to explain glucolipotoxicity-induced β-cell dysfunction and death, but its major factors appear to be depression of key transcription factor gene expression by altered intracellular energy metabolism and oxidative stress. Therefore, stabilization of metabolic changes induced by glucolipotoxicity in β-cells represents a new avenue for the treatment of type 2 diabetes mellitus.


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