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Hormones Regulating Blood Glucose01:16

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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A Model of Chronic Nutrient Infusion in the Rat
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Insulin Modulates Liver Function in a Type I Diabetes Rat Model.

Eduardo L Nolasco, Fernando L Zanoni, Fernanda P B Nunes

    Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
    |July 11, 2015
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    Summary

    Insulin treatment in diabetic rats undergoing cecal ligation and puncture (CLP) partially restored liver function and attenuated peritoneal inflammation. This suggests insulin may mitigate sepsis-related complications in diabetic individuals.

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    Area of Science:

    • Endocrinology
    • Immunology
    • Sepsis Research

    Background:

    • Diabetes mellitus is linked to increased infection susceptibility.
    • Cecal ligation and puncture (CLP) is a model for polymicrobial sepsis.
    • The impact of insulin on the inflammatory response in diabetic sepsis models requires further investigation.

    Purpose of the Study:

    • To investigate the effect of insulin on the local inflammatory environment following CLP in diabetic rats.
    • To assess insulin's role in mitigating organ dysfunction during sepsis in a diabetic context.

    Main Methods:

    • Diabetic and non-diabetic rats underwent a two-puncture CLP procedure.
    • Peritoneal lavage (PeL) and bronchoalveolar lavage (BAL) fluids were analyzed for cell counts and cytokine levels (TNF-α, IL-1β, IL-6, IL-10, CINC-1, CINC-2) via ELISA.
    • Biochemical parameters (urea, creatinine, ALT, AST, ALP) and organ morphology were assessed.
    • Insulin (NPH) was administered to diabetic rats before CLP.

    Main Results:

    • CLP increased inflammatory cells and cytokines in PeL fluid in both diabetic and non-diabetic rats.
    • Insulin treatment in diabetic rats increased PeL fluid cells but did not alter cytokine levels.
    • Diabetic CLP rats showed elevated liver enzymes (ALT, AST, ALP) and urea compared to non-diabetic CLP rats.
    • Insulin treatment normalized ALT, AST, and ALP levels in diabetic rats.

    Conclusions:

    • Insulin treatment attenuates liver dysfunction in diabetic rats with early CLP-induced peritoneal inflammation.
    • Insulin may play a protective role against organ damage during sepsis in diabetic individuals.
    • Further research is warranted to explore insulin's therapeutic potential in sepsis management for diabetic patients.