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Related Concept Videos

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Pathophysiology of Diabetes

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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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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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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Glucose Homeostasis: Regulation of Blood Glucose01:02

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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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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
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A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta
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Elevated Glucose and Insulin Levels Decrease DHA Transfer across Human Trophoblasts via SIRT1-Dependent Mechanism.

Jay S Mishra1, Hanjie Zhao1, Sari Hattis1

  • 1Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706, USA.

Nutrients
|May 6, 2020
PubMed
Summary
This summary is machine-generated.

Gestational diabetes mellitus (GDM) impairs fetal docosahexaenoic acid (DHA) transfer by reducing placental Sirtuin-1 (SIRT1). Restoring SIRT1 function may improve DHA levels in fetuses of GDM mothers.

Keywords:
CD36DHAFABP3FABP4SIRT1fatty acid transportgestational diabeteslipid metabolismtrophoblast

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In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
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Area of Science:

  • Obstetrics and Gynecology
  • Metabolic Disorders
  • Molecular Biology

Background:

  • Gestational diabetes mellitus (GDM) is linked to reduced fetal docosahexaenoic acid (DHA) transfer, potentially due to placental dysfunction.
  • Sirtuin-1 (SIRT1) is a key nutrient sensor involved in regulating lipid metabolism.

Purpose of the Study:

  • To investigate how GDM-related high glucose and insulin conditions affect DHA transfer and fatty acid transporter expression.
  • To determine the role of Sirtuin-1 (SIRT1) in regulating DHA transfer under GDM conditions.

Main Methods:

  • Primary human trophoblasts were cultured and exposed to high glucose and insulin to simulate GDM.
  • DHA transfer, triglyceride accumulation, fatty acid transporter expression (CD36, FABP3, FABP4), and SIRT1 expression were measured.
  • The effects of a SIRT1 inhibitor, recombinant SIRT1, and SIRT1 activators on DHA transfer were assessed.

Main Results:

  • GDM conditions significantly decreased DHA transfer across trophoblasts.
  • GDM conditions increased triglyceride accumulation and fatty acid transporter expression but suppressed SIRT1 expression.
  • SIRT1 inhibition reduced DHA transfer, while SIRT1 restoration normalized DHA transport in GDM conditions.

Conclusions:

  • Sirtuin-1 (SIRT1) plays a critical role in regulating placental DHA transfer.
  • Suppressed SIRT1 expression in GDM contributes to reduced fetal DHA supply, offering new molecular insights into GDM's impact on fetal development.