Early postnatal nutrition is involved in metabolic programming, an excess of protein being suspected to enhance early growth and the propensity to later develop insulin resistance and type 2 diabetes mellitus. The aim of the present study was to test the hypothesis that excessive protein intake during the suckling period would overstimulate the endocrine pancreas in the short term and alter durably its maturation, contributing to the later disruption of glucose homeostasis. Normal-birth-weight and low-birth-weight piglets were fed isoenergetic formulae providing an adequate-protein (AP, equivalent to sow milk) or a high-protein (HP, +48 %) supply between 7 and 28 d of age and were fed a standard diet until 70 d of age. During the formula-feeding period, the HP formula did not modify postprandial insulin secretion but transiently increased fasting insulin and the homeostasis model assessment-insulin resistance index (HOMA-IR, P < 0·05). Fasting insulin and HOMA-IR were restored to AP piglets' values 1 month after weaning. The structure of the endocrine pancreas was not affected by the protein content of the formula. The weight at birth had no major effect on the studied parameters. We concluded that a high-protein supply during the suckling period does not interfere with insulin secretion and endocrine pancreas maturation in the short term. It has no consequences either on glucose tolerance 1 month after weaning. The present study demonstrated that up-regulation of postprandial insulin secretion is not involved in higher growth observed in piglets fed a HP formula.
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http://dx.doi.org/10.1017/S0007114511005253 | DOI Listing |
ACS Meas Sci Au
December 2024
Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Medicinaregatan 11-13, 41390 Gothenburg, Sweden.
Single cell Amperometry (SCA) is a powerful, sensitive, high temporal resolution electrochemical technique used to quantify secreted molecular messengers from individual cells and vesicles. This technique has been extensively applied to study the process of exocytosis, and it has also been applied, albeit less frequently, to investigate insulin exocytosis from single pancreatic beta cells. Insufficient insulin release can lead to diabetes, a chronic lifestyle disorder that affects millions of people worldwide.
View Article and Find Full Text PDFJ Diabetes Metab Disord
June 2025
Department of Clinical Sciences in Malmö, Lund University, Lund, Sweden.
Background: Middle Eastern (ME) immigrants to Europe have a heavy burden of metabolic disorders including a higher prevalence of insulin resistance, T2D and obesity as compared to native-born Europeans. Vitamin D insufficiency and deficiency are prevalent conditions in people originating from the ME.
Aims: To study the differences in the levels of 25(OH)D and parathyroid hormone (PTH) across ME and European ethnicity, and the effect of 25(OH)D and PTH on insulin action and secretion.
Front Med (Lausanne)
December 2024
Department of Medical Laboratory Science, College of Medicine and Health Sciences, Jigjiga University, Jigjiga, Ethiopia.
Introduction: Diabetes Mellitus (DM) is a disorder of multiple etiologies characterized by chronic hyperglycemia resulting from defects in insulin secretion and/or insulin action. DM patients have a disturbance of hemostasis, leading to a prothrombotic state characterized by platelet hypersensitivity, coagulation factor disorders, and hypo-fibrinolysis. Therefore, the primary goal of this systematic review and meta-analysis was to determine the pooled Standard Mean Difference (SMD) of prothrombin time (PT) and activated partial thromboplastin time (APTT) of DM patients in Africa.
View Article and Find Full Text PDFMonogenic diabetes, formerly called Maturity-Onset Diabetes of the Young (MODY), involves single-gene mutations, typically with dominant inheritance, and has been associated with variants in 14 genes. Among these, mutations are the most common, and their diagnosis allows the use of alternative therapies, including sulfonylureas. In an earlier study, we described a variant displaying recessive transmission, p.
View Article and Find Full Text PDFMetabolism
December 2024
Department of Pharmacology, Weill Cornell Medicine, New York, NY 10021, United States of America.
Aims: NAD deficiency underlies obesity-induced metabolic disturbances. This study evaluated dihydronicotinamide riboside (NRH), a potent NAD enhancer, in lean and obese mice and explored whether NRH operates through a unique mechanism involving adenosine kinase (ADK), an enzyme critical for NRH-driven NAD synthesis.
Methods: Pharmacokinetic and pharmacodynamic analyses were performed following a single 250 mg/kg intraperitoneal injection of NRH in healthy mice.
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