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Open AccessArticle

Jejunal Insulin Signalling Is Increased in Morbidly Obese Subjects with High Insulin Resistance and Is Regulated by Insulin and Leptin

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Instituto de Investigación Biomédica de Málaga-IBIMA, 29009 Málaga, Spain
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Unidad de Gestión Clínica de Endocrinología y Nutrición, Hospital Universitario Virgen de la Victoria, 29009 Málaga, Spain
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Unidad de Gestión Clínica de Aparato Digestivo, Hospital Universitario Virgen de la Victoria, 29009 Málaga, Spain
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Facultad de Ciencias, Universidad de Málaga, 29009 Málaga, Spain
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Facultad de Medicina, Universidad de Málaga, 29009 Málaga, Spain
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Unidad de Gestión Clínica de Endocrinología y Nutrición, Hospital Regional Universitario, 29009 Málaga, Spain
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CIBER de Diabetes y Enfermedades Metabólicas Asociadas-CIBERDEM, 29009 Málaga, Spain
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CIBER Fisiopatología de la Obesidad y Nutrición-CIBEROBN, 29009 Málaga, Spain
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Unidad de Gestión Clínica de Cirugía General, Digestiva y Trasplantes, Hospital Regional Universitario, 29009 Málaga, Spain
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Institut National de la Santé et de la Recherche Médicale, U1213, F-69008 Lyon, France
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Université de Lyon, F-69008 Lyon, France
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Faculté Lyon-Est Laennec, Université de Lyon 1, F-69622 Villeurbanne, France
*
Authors to whom correspondence should be addressed.
J. Clin. Med. 2020, 9(1), 196; https://doi.org/10.3390/jcm9010196 (registering DOI)
Received: 18 November 2019 / Revised: 16 December 2019 / Accepted: 3 January 2020 / Published: 10 January 2020
(This article belongs to the Section Endocrinology & Metabolism)
Little is known about the jejunal insulin signalling pathways in insulin resistance/diabetes states and their possible regulation by insulin/leptin. We study in jejunum the relation between insulin signalling and insulin resistance in morbidly obese subjects with low (MO-low-IR) or with high insulin resistance (MO-high-IR), and with type 2 diabetes treated with metformin (MO-metf-T2DM), and the effect of insulin/leptin on intestinal epithelial cells (IEC). Insulin receptor substrate-1 (IRS1) and the catalytic p110β subunit (p110β) of phosphatidylinositol 3-kinase (PI3K) were higher in MO-high-IR than in MO-low-IR. The regulatory p85α subunit of PI3K (p85α)/p110β ratio was lower in MO-high-IR and MO-metf-T2DM than in MO-low-IR. Akt-phosphorylation in Ser473 was reduced in MO-high-IR compared with MO-low-IR. IRS1 and p110-β were associated with insulin and leptin levels. The improvement of body mass index (BMI) and HOMA-IR (homeostasis model assessment of insulin resistance index) after bariatric surgery was associated with a higher IRS1 and a lower p85α/p110β ratio. IEC (intestinal epithelial cells) incubation with a high glucose + insulin dose produced an increase of p85α and p110β. High dose of leptin produced an increase of IRS1, p85α and p110β. In conclusion, despite the existence of insulin resistance, the jejunal expression of genes involved in insulin signalling was increased in MO-high-IR. Their expressions were regulated mainly by leptin. IRS1 and p85α/p110β ratio was associated with the evolution of insulin resistance after bariatric surgery. View Full-Text
Keywords: insulin resistance; jejunum; morbid obesity; leptin insulin resistance; jejunum; morbid obesity; leptin
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Gutierrez-Repiso, C.; Ho-Plagaro, A.; Santiago-Fernandez, C.; Garcia-Serrano, S.; Rodríguez-Pacheco, F.; Valdes, S.; Garrido-Sanchez, L.; Rodríguez-Díaz, C.; López-Gómez, C.; Moreno-Ruiz, F.J.; Alcain-Martinez, G.; Gautier-Stein, A.; Mithieux, G.; Garcia-Fuentes, E. Jejunal Insulin Signalling Is Increased in Morbidly Obese Subjects with High Insulin Resistance and Is Regulated by Insulin and Leptin. J. Clin. Med. 2020, 9, 196.

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