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Related Concept Videos

Metabolic States of the Body: Fasting and Starvation01:24

Metabolic States of the Body: Fasting and Starvation

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...
Metabolic States of the Body: The Postabsorptive State01:18

Metabolic States of the Body: The Postabsorptive State

The postabsorptive state usually starts about four hours after a meal and lasts until the next meal is eaten. During this time, the digestive system stops absorbing nutrients, and the body uses stored energy reserves to maintain stable blood glucose levels.
Initially, glycogen stored in the liver is broken down to release glucose into the bloodstream, while glycogen in the muscles is broken down to supply glucose for energy directly within the muscle cells. As glycogen stores diminish,...
Pathophysiology of Vomiting01:22

Pathophysiology of Vomiting

Vomiting is a complex physiological response to expel harmful or irritating substances from the body. It's a defensive mechanism triggered by stimuli like poisons, microbial toxins, cytotoxic drugs, and mechanical abdominal distension. The process is centrally coordinated by the vomiting (or emetic) center located in the medulla of the brainstem. This area, rich in muscarinic M1, histamine H1, neurokinin 1 (NK1), and serotonin 5-HT3 receptors, coordinates the act of vomiting through interaction...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

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...
Glucose Homeostasis: Regulation of Blood Glucose01:02

Glucose Homeostasis: Regulation of Blood Glucose

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.
During fasting, when blood glucose levels are low, the pancreas secretes glucagon. it...

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3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
10:39

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Published on: June 2, 2014

How does fasting trigger migraine? A hypothesis.

Turgay Dalkara1, Kivilcim Kiliç

  • 1Institute of Neurological Sciences and Psychiatry, Hacettepe University, Ankara, Turkey. tdalkara@hacettepe.edu.tr

Current Pain and Headache Reports
|September 3, 2013
PubMed
Summary
This summary is machine-generated.

Fasting can trigger migraines by depleting brain glucose stores, leading to neuronal imbalances. This may activate pain pathways, potentially causing migraine headaches with or without aura.

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Area of Science:

  • Neuroscience
  • Metabolic disorders
  • Neurology

Background:

  • Fasting and skipped meals are known migraine triggers.
  • The precise mechanisms behind fasting-induced migraines remain largely unknown.
  • Brain glycogen metabolism and its interaction with sympathetic activity are critical areas of research.

Purpose of the Study:

  • To review recent advancements in brain glycogen metabolism.
  • To propose a novel mechanism for fasting-induced migraine headaches.
  • To explore the role of synaptic activity and neuronal depolarization in migraine pathogenesis.

Main Methods:

  • Literature review of recent developments in brain glycogen metabolism.
  • Analysis of sympathetic activity's role in modulating brain glucose supply.
  • Hypothesizing the sequence of events from glucose deficiency to trigeminal nerve activation.

Main Results:

  • Insufficient glycogen-derived glucose during intense synaptic activity may disrupt neuronal and astrocyte balance.
  • This imbalance can lead to collective network depolarization.
  • Activated pannexin1 channels and inflammatory pathways may trigger perivascular trigeminal afferents.

Conclusions:

  • Fasting-induced migraines may stem from inadequate brain glucose supply.
  • Network depolarization, influenced by glucose availability, is a potential migraine trigger.
  • The spread of network depolarization could differentiate between migraine with and without aura.