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Related Concept Videos

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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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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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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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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
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Related Experiment Video

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Ketone-Based Alert System for Insulin Pump Failures.

Eleonora M Aiello1,2, Lori M Laffel3, Mary-Elizabeth Patti3

  • 1Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Allston, MA, USA.

Journal of Diabetes Science and Technology
|November 10, 2023
PubMed
Summary
This summary is machine-generated.

A new ketone-based alert system (K-AS) rapidly detects insulin pump failures in type 1 diabetes (T1D) by monitoring 3-beta-hydroxybutyrate (BOHB) levels. This system aims to prevent diabetic ketoacidosis (DKA) with faster alerts than current guidelines.

Keywords:
Kalman filterketone measurementpump failuretype 1 diabetes

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Area of Science:

  • Biomedical Engineering
  • Endocrinology
  • Diabetes Technology

Background:

  • Type 1 diabetes (T1D) management often involves insulin pumps.
  • Insulin delivery interruptions can quickly lead to diabetic ketoacidosis (DKA).
  • Early detection of insulin cessation is critical for patient safety.

Purpose of the Study:

  • To develop and evaluate a ketone-based alert system (K-AS) for detecting accidental insulin delivery cessation.
  • To improve the speed of DKA prevention in individuals with T1D using insulin pumps.

Main Methods:

  • Designed a K-AS utilizing an extended Kalman filter and plasma 3-beta-hydroxybutyrate (BOHB) measurements.
  • Developed a novel physiological model simulating ketone body turnover in response to insulin level changes.
  • Validated the K-AS using the S2014 UVA/Padova simulator on 10 in silico subjects.

Main Results:

  • The K-AS achieved average detection times of 84 minutes (fasting) and 55.5 minutes (postprandial).
  • These detection times represent a significant improvement over current guideline-based detection times (193 and 120 minutes, respectively).

Conclusions:

  • The K-AS effectively uses the rapid increase in plasma BOHB for early DKA risk detection.
  • The system provides timely alerts without false positives, enhancing patient safety.
  • The novel insulin-BOHB model aids in understanding treatment efficacy safely.