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Related Concept Videos

Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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Oral Hypoglycemic Agents: Glinides01:06

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Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
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Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

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Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
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Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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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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Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
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A PID Control Algorithm for a Post-Prandial Hypoglycemic Clamp Study.

J Pavan, C Dalla Man, D Herzig

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    Summary
    This summary is machine-generated.

    A new PID algorithm aids in safely and accurately controlling blood glucose levels during postprandial hypoglycemia studies, particularly for patients with post-bariatric hypoglycemia (PBH). This tool ensures precise target achievement in research settings.

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    Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
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    Area of Science:

    • Metabolic Disorders and Endocrinology
    • Computational Physiology and Control Systems

    Background:

    • Post-prandial hypoglycemia (PPHG) is a metabolic complication following bariatric surgery (PBH), with unclear underlying mechanisms.
    • Existing manual methods for postprandial hypoglycemic clamp procedures are challenging and pose safety risks due to potential glycemic undershoots.
    • Impaired counter-regulation is a suspected pathophysiological feature of PPHG, necessitating standardized clamp studies.

    Purpose of the Study:

    • To develop and evaluate a Proportional-Integral-Derivative (PID) control algorithm for assisting in standardized postprandial hypoglycemic clamp procedures.
    • To enable accurate and safe achievement of predefined blood glucose (BG) trajectories and hypoglycemic targets in research settings.
    • To test the algorithm's robustness against various sources of variability and errors in simulated physiological conditions.

    Main Methods:

    • Development of a PID algorithm designed to assist in adjusting glucose infusion rate (GIR) for BG clamping.
    • In silico testing of the PID controller simulating glucose-insulin dynamics in both post-bariatric hypoglycemia (PBH) patients and healthy controls.
    • Simulation of diverse scenarios to assess algorithm robustness against BG measurement outliers, sampling delays, and missed measurements.

    Main Results:

    • The PID algorithm demonstrated capability in accurately and safely reaching target BG levels in simulated PBH subjects (median deviation 2.4%) and healthy controls (median deviation 2.8%).
    • The controller performed robustly across various simulated error conditions, including outliers, delays, and missed measurements.
    • The algorithm's manual mode allows for investigator intervention, enhancing safety and flexibility during clamp procedures.

    Conclusions:

    • The developed PID control algorithm facilitates standardized, accurate, and safe postprandial hypoglycemic clamp procedures.
    • This computational tool is effective in both healthy individuals and those with post-bariatric hypoglycemia (PBH).
    • The algorithm represents a significant advancement for investigating the pathophysiology of post-prandial hypoglycemia.