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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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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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Regulation of Food Intake01:30

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Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
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Metabolic States of the Body: Fasting and Starvation01:24

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During the initial hours of fasting, the body uses up its glycogen stores as an energy source. Once these glycogen reserves are depleted, the body begins breaking down stored triglycerides and structural proteins. During this stage, glycerol becomes a key substrate for gluconeogenesis, while free fatty acids undergo beta-oxidation to provide energy for tissues, such as skeletal muscle. In the fasting state, the body spares protein breakdown as much as possible to conserve muscle and structural...
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Stress-level glucocorticoids increase fasting hunger and decrease cerebral blood flow in regions regulating eating.

Jason Bini1, Lisa Parikh2, Cheryl Lacadie1

  • 1Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, United States.

Neuroimage. Clinical
|September 20, 2022
PubMed
Summary
This summary is machine-generated.

Elevated glucocorticoids, similar to stress levels, increase hunger and reduce brain blood flow in key appetite control regions. This suggests a link between stress hormones, brain function, and appetite regulation, potentially contributing to obesity.

Keywords:
CortisolGlucocorticoidsHungerStressfMRI

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Area of Science:

  • Neuroendocrinology
  • Metabolic Regulation
  • Neuroimaging

Background:

  • Appetite and energy homeostasis are regulated by neural pathways that overlap with stress neurobiology.
  • Chronic stress can dysregulate the cortico-limbic striatal system, impairing the integration of homeostatic and hedonic food intake signals.
  • Understanding stress-induced appetite alterations is crucial for addressing weight gain.

Purpose of the Study:

  • To investigate the effects of glucocorticoids on metabolic, neural, and behavioral factors related to appetite and obesity risk.
  • To determine how stress hormones influence brain activity and hunger signaling.

Main Methods:

  • Randomized, double-blind, cross-over study involving overnight hydrocortisone or saline infusion.
  • Fasting perfusion magnetic resonance imaging (MRI) to assess regional cerebral blood flow (CBF).
  • Measurements included Visual Analog Scale (VAS) for hunger, cortisol, and metabolic hormones.

Main Results:

  • Hydrocortisone infusion decreased CBF in the hypothalamus and cortico-striatal-limbic regions compared to saline.
  • Hunger ratings, insulin, glucose, and leptin levels were significantly increased by hydrocortisone.
  • Reduced CBF in specific brain areas (medial OFC, brainstem, thalamus) predicted increased hunger, which was associated with plasma insulin.

Conclusions:

  • Glucocorticoid levels mimicking psychological stress increase fasting hunger.
  • Decreased regional CBF in brain networks controlling food intake is observed.
  • These findings link stress hormones, brain function, and appetite regulation, offering insights into obesity risk.