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      Long-term increase of insulin secretion in mice subjected to pregnancy and lactation

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          Abstract

          Purpose

          Observational studies show that longer breastfeeding periods reduce maternal risk of type 2 diabetes mellitus. However, it is currently unknown if the long-term benefits of breastfeeding for maternal glucose homeostasis are linked to changes in the endocrine pancreas.

          Methods

          We presently evaluated functional, morphological and molecular aspects of the endocrine pancreas of mice subjected to two sequential cycles of pregnancy and lactation (L21). Age-matched mice not allowed to breastfeed (L0) and virgin mice were used as controls.

          Results

          L21 mice exhibited increased tolerance and increased glucose-stimulated insulin secretion (GSIS) by isolated islets. Pancreatic islets of L21 mice did not present evident morphological changes to justify the increased GSIS. On the other hand, islets of L21 mice exhibited a reduction in Cavb3 and Kir6.2 expression with concordant increased intracellular Ca 2+ levels after challenge with glucose.

          Conclusion

          Altogether, the present findings show the breastfeeding exerts long-term benefits for maternal endocrine pancreas by increasing intracellular Ca 2+ levels and GSIS.

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          Most cited references30

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          Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.

          Patrik Rorsman, Frances M. Ashcroft (2018)
          The pancreatic β-cell plays a key role in glucose homeostasis by secreting insulin, the only hormone capable of lowering the blood glucose concentration. Impaired insulin secretion results in the chronic hyperglycemia that characterizes type 2 diabetes (T2DM), which currently afflicts >450 million people worldwide. The healthy β-cell acts as a glucose sensor matching its output to the circulating glucose concentration. It does so via metabolically induced changes in electrical activity, which culminate in an increase in the cytoplasmic Ca2+ concentration and initiation of Ca2+-dependent exocytosis of insulin-containing secretory granules. Here, we review recent advances in our understanding of the β-cell transcriptome, electrical activity, and insulin exocytosis. We highlight salient differences between mouse and human β-cells, provide models of how the different ion channels contribute to their electrical activity and insulin secretion, and conclude by discussing how these processes become perturbed in T2DM.
          Article 0 comments Cited 304 times – based on 0 reviews     Review now
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            Comparison of abdominal adiposity and overall obesity in predicting risk of type 2 diabetes among men.

            Youfa Wang, Eric Rimm, Meir J. Stampfer … (2005)
            Obesity is a strong risk factor for type 2 diabetes. However, few studies have compared the predictive power of overall obesity with that of central obesity. The cutoffs for waist circumference (WC) and waist-to-hip ratio (WHR) as measures of abdominal adiposity remain controversial. The objective was to compare body mass index (BMI), WC, and WHR in predicting type 2 diabetes. A prospective cohort study (Health Professionals Follow-Up Study) of 27 270 men was conducted. WC, WHR, and BMI were assessed at baseline. Covariates and potential confounders were assessed repeatedly during the follow-up. During 13 y of follow-up, we documented 884 incident type 2 diabetes cases. Age-adjusted relative risks (RRs) across quintiles of WC were 1.0, 2.0, 2.7, 5.0, and 12.0; those of WHR were 1.0, 2.1, 2.7, 3.6, and 6.9; and those of BMI were 1.0, 1.1, 1.8, 2.9, and 7.9 (P for trend /=24.8), WC (>/=94 cm), and WHR (>/=0.94) were 82.5%, 83.6%, and 74.1%, respectively. The corresponding proportions were 78.9%, 50.5%, and 65.7% according to the recommended cutoffs. Both overall and abdominal adiposity strongly and independently predict risk of type 2 diabetes. WC is a better predictor than is WHR. The currently recommended cutoff for WC of 102 cm for men may need to be reevaluated; a lower cutoff may be more appropriate.
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              RNA sequencing identifies dysregulation of the human pancreatic islet transcriptome by the saturated fatty acid palmitate.

              Miriam Cnop, Baroj Abdulkarim, Guy Bottu … (2014)
              Pancreatic β-cell dysfunction and death are central in the pathogenesis of type 2 diabetes (T2D). Saturated fatty acids cause β-cell failure and contribute to diabetes development in genetically predisposed individuals. Here we used RNA sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes. Palmitate induced fatty acid metabolism and endoplasmic reticulum (ER) stress. Functional studies identified novel mediators of adaptive ER stress signaling. Palmitate modified genes regulating ubiquitin and proteasome function, autophagy, and apoptosis. Inhibition of autophagic flux and lysosome function contributed to lipotoxicity. Palmitate inhibited transcription factors controlling β-cell phenotype, including PAX4 and GATA6. Fifty-nine T2D candidate genes were expressed in human islets, and 11 were modified by palmitate. Palmitate modified expression of 17 splicing factors and shifted alternative splicing of 3,525 transcripts. Ingenuity Pathway Analysis of modified transcripts and genes confirmed that top changed functions related to cell death. Database for Annotation, Visualization and Integrated Discovery (DAVID) analysis of transcription factor binding sites in palmitate-modified transcripts revealed a role for PAX4, GATA, and the ER stress response regulators XBP1 and ATF6. This human islet transcriptome study identified novel mechanisms of palmitate-induced β-cell dysfunction and death. The data point to cross talk between metabolic stress and candidate genes at the β-cell level.
              Article 0 comments Cited 131 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocr Connect
                Journal ID (iso-abbrev): Endocr Connect
                Journal ID (hwp): EC
                Title: Endocrine Connections
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Electronic): 2049-3614
                Publication date Collection: April 2020
                Publication date (Electronic): 17 March 2020
                Volume: 9
                Issue: 4
                Pages: 299-308
                Affiliations
                [1 ]Department of Pharmacology , Faculty of Medical Sciences, State University of Campinas, Campinas, Brazil
                [2 ]Department of Structural and Functional Biology , Institute of Biology, State University of Campinas, Campinas, Brazil
                [3 ]Department of Genetics , Evolution, Microbiology and Immunology, Institute of Biology, State University of Campinas, Campinas, Brazil
                [4 ]Department of Physiology and Biophysics , Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil
                Author notes
                Correspondence should be addressed to G F Anhe: anhegf@ 123456fcm.unicamp.br
                Author information
                http://orcid.org/0000-0002-4951-1130
                Article
                Publisher ID: EC-20-0020
                DOI: 10.1530/EC-20-0020
                PMC ID: 7159261
                PubMed ID: 32182583
                SO-VID: 53507890-88d9-41ce-a382-400d3a64ebd0
                Copyright © © 2020 The authors
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                Date received : 17 February 2020
                Date accepted : 17 March 2020
                Categories
                Subject: Research

                Keywords: pregnancy,lactation,pancreatic islets,insulin secretion,type 2 diabetes mellitus
                Data availability:
                Keywords: pregnancy, lactation, pancreatic islets, insulin secretion, type 2 diabetes mellitus

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