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Related Concept Videos

Pathophysiology of Diabetes01:20

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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Glucose Transporters01:27

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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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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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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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Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
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Maternal Obesity Programs Glucose Intolerance in Pregnant Female Offspring.

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Maternal obesity in mice leads to impaired pregnancy metabolism in female offspring, causing insulin insufficiency and disrupted lipid homeostasis. This may create a transgenerational cycle of metabolic dysfunction, increasing risks for future generations.

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Area of Science:

  • Metabolic Health
  • Reproductive Biology
  • Developmental Origins of Health and Disease

Background:

  • Maternal obesity is a significant risk factor for offspring metabolic dysfunction.
  • The specific impact of maternal obesity on the metabolic adaptation to pregnancy in female offspring is not well understood.

Purpose of the Study:

  • To investigate the effects of maternal high-fat (HF) diet-induced obesity on the metabolic adaptation to pregnancy in female offspring.
  • To explore potential transgenerational effects on metabolic health.

Main Methods:

  • Utilized a mouse model (C57BL/6J) where dams were fed either a high-fat (HF) diet or a control chow diet before and during pregnancy.
  • Assessed fetal growth, postnatal development, adult adiposity, and metabolic parameters (glucose, insulin, triglycerides) during pregnancy in female offspring.
  • Examined glucose-stimulated insulin secretion and beta-cell function in cultured islets from pregnant female offspring.

Main Results:

  • Female offspring of HF-fed dams (OF-HFD) showed reduced fetal growth, followed by catch-up growth and increased adult adiposity.
  • During pregnancy, OF-HFD exhibited impaired metabolic adaptations, including diminished increases in body fat and triglycerides, glucose intolerance, and reduced insulin secretion despite normal beta-cell mass.
  • Hepatic triglyceride secretion was decreased, and liver insulin signaling was enhanced in pregnant OF-HFD, indicating altered lipid and glucose metabolism.

Conclusions:

  • Maternal obesity significantly impairs the metabolic adaptation to pregnancy in female offspring, leading to insulin insufficiency and disrupted lipid homeostasis.
  • These metabolic alterations in female offspring may contribute to a transgenerational cycle of metabolic dysfunction, potentially increasing the risk of gestational diabetes.
  • Findings highlight the need for interventions to mitigate the long-term metabolic consequences of maternal obesity across generations.