Starvation State
Starvation State - Related Videos
09:24
An Anoxia-starvation Model for Ischemia/Reperfusion in C. elegans
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Cited by 4 •
2014
A protocol is described that uses anoxia/starvation in C. elegans to model ischemia/reperfusion. Functional outcomes include increased mortality, visible abnormalities in GFP-labeled neuronal processes, and impaired behavioral responses that require neuronal function.
06:51
Analysis of Autophagy in Penicillium chrysogenum by Using Starvation Pads in Combination With Fluorescence Microscopy
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Cited by 2 •
2015
A convenient and powerful method for studying autophagy in Penicillium chrysogenum by using starvation pads (mixtures of agarose and tap water in a microscope slide containing a central cavity) is presented here.
01:24
Metabolic States of the Body: Fasting and Starvation
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2024
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...
07:48
Investigating the Function of Coronin A in the Early Starvation Response of Dictyostelium discoideum by Aggregation Assays
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Cited by 1 •
2016
The social amoeba Dictyostelium discoideum undergoes a developmental transition into a multicellular organism when starved. The evolutionary conserved protein coronin A plays a crucial role in the initiation of development. Using aggregation assays as our main method, we aim to elucidate the role of coronin A in early development.
11:53
Derivation of Highly Purified Cardiomyocytes from Human Induced Pluripotent Stem Cells Using Small Molecule-modulated Differentiation and Subsequent Glucose Starvation
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Cited by 113 •
2015
Here, we describe a robust protocol for human cardiomyocyte derivation that combines small molecule-modulated cardiac differentiation and glucose deprivation-mediated cardiomyocyte purification, enabling production of purified cardiomyocytes for the purposes of cardiovascular disease modeling and drug screening.
FAQs
Declining glucose availability reduces insulin signaling and increases glucagon signaling. This hormonal shift coordinates several metabolic responses rather than activating a single pathway: glycogen breakdown releases stored glucose, gluconeogenesis supports continued glucose production, and lipolysis mobilizes fatty acids. Together, these changes redirect fuel use as the body adapts to limited nutrient intake.
These pathways address different energy requirements during nutrient scarcity. Glycogen breakdown provides access to stored carbohydrate, gluconeogenesis generates glucose when carbohydrate availability falls, and lipolysis releases fatty acids for energy production. Their coordinated activation helps maintain glucose availability while increasing reliance on non-carbohydrate fuels, allowing metabolism to respond to changing energy demands.
As lipolysis increases, fatty acids supply the liver with more acetyl-CoA. The liver converts this acetyl-CoA into ketone bodies, creating an alternative circulating fuel when glucose availability is reduced. Ketone production therefore links increased fat mobilization with broader energy distribution and helps support tissues while limiting the need to use available glucose.
Ketone bodies provide energy to tissues that can use them, reducing overall dependence on glucose during prolonged nutrient limitation. This redistribution matters because some cells remain glucose-dependent. By supplying an alternative fuel to other tissues, ketone metabolism helps conserve glucose for those cells and forms part of the organism’s broader energy-homeostasis response.
Researchers study this state to examine coordinated changes in energy homeostasis, including altered hormone signaling, carbohydrate mobilization, fat use, and ketone production. The model helps connect molecular metabolic pathways with physiological adaptation. It is relevant to investigations of fasting, malnutrition, metabolic disease, and the biological capacity to tolerate limited nutrient availability.
A useful analysis considers the shift from glucose use toward fat and ketone metabolism, along with the signaling changes that initiate it. Researchers can examine glycogen breakdown, gluconeogenesis, lipolysis, fatty-acid-derived acetyl-CoA, and hepatic ketone-body production as linked events. This integrated view is more informative than treating each pathway as an isolated response.