Diet-induced Obesity
Diet-induced Obesity - Related Videos
02:31
Detection of Orexin and Cannabinoid Receptor Co-localization in Diet-Induced Obese Zebrafish
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2025
This video demonstrates a protocol for investigating the co-localization of orexin and cannabinoid receptors in normal and diet-induced obesity (DIO) adult zebrafish brain tissue using immunofluorescence.
09:10
Palatable Western-style Cafeteria Diet as a Reliable Method for Modeling Diet-induced Obesity in Rodents
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Cited by 42 •
2019
This protocol describes the use of a highly palatable, western-style cafeteria diet to model overeating and obesity in rodents. Here, we provide a detailed outline of food selection, preparation and measurement, and explain methodological factors that assist in generating a robust and reproducible phenotype.
08:50
Duodenal-Jejunal Bypass Surgery in Diet-Induced Obese Diabetic Mice
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2024
Duodenal-jejunal bypass (DJB) surgery can improve glucose metabolism and reduce insulin resistance. Here, we present a protocol to establish a stable and reliable mouse model of DJB.
06:28
A Chronic High-Intensity Interval Training and Diet-Induced Obesity Model to Maximize Exercise Effort and Induce Physiologic Changes in Rats
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Cited by 3 •
2023
This paper presents the morphometric responses and training performance outcomes of a high-intensity interval training (HIIT) protocol in a Sprague-Dawley rat model of diet-induced obesity. The purpose of this protocol was to maximize exercise intensity and determine the physiologic responses to HIIT in lean and obese rats.
09:15
Vinyl Chloride and High-Fat Diet as a Model of Environment and Obesity Interaction
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Cited by 8 •
2020
The goal of this protocol was to develop a murine model of low-level toxicant exposure that does not cause overt liver injury but rather exacerbates pre-existing liver damage. This paradigm better recapitulates human exposure and the subtle changes that occur upon exposure to toxicant concentrations that are considered safe.
FAQs
Leptin and insulin normally convey information about energy stores and nutrient availability to hypothalamic circuits that influence appetite and energy expenditure. With chronic overnutrition, these signals become disrupted, weakening the neural representation of satiety. This helps researchers connect altered hormonal communication with persistent feeding, reduced metabolic control, and changes in brain regulation of body weight.
Chronic overnutrition can trigger neuroinflammation, adding an inflammatory component to the metabolic changes caused by excess energy intake. Researchers can therefore examine how nutritional stress affects neural signaling alongside appetite and energy regulation. This perspective is useful for investigating whether inflammatory brain changes contribute to weakened satiety signaling, behavioral alterations, or broader neurological consequences.
The model allows researchers to study feeding as both a metabolic response and a behavior influenced by reward. Metabolic control concerns signals that regulate energy balance, whereas reward-driven feeding emphasizes the motivational effects of energy-dense food. Examining both dimensions helps explain why altered brain function may sustain food intake even when normal satiety signaling is weakened.
A useful assessment spans several levels: adipose tissue expansion, metabolic changes, hormonal signaling, feeding behavior, and brain function. Researchers may also examine satiety responses, reward-related behavior, cognitive changes, or indicators of neuroinflammation. Considering these outcomes together helps determine whether an intervention changes body metabolism alone or also modifies neural and behavioral consequences.
Studies establish the model through sustained consumption of energy-dense food and then evaluate consequences across metabolic, behavioral, and neural domains. Measurements can be organized around adipose tissue, appetite-related hormonal signals, energy expenditure, feeding behavior, and brain function. This coordinated approach links the nutritional exposure to specific physiological and neuroscience outcomes rather than relying on body-weight change alone.
The model supports testing behavioral, pharmacological, and nutritional interventions. Outcomes can be compared across appetite regulation, energy expenditure, reward-driven feeding, cognitive changes, hormonal signaling, and neuroinflammation. Its value lies in revealing whether a treatment affects only metabolic features or also improves disrupted communication between nutritional signals and brain circuits involved in feeding and energy balance.
Because chronic overnutrition can influence brain function as well as metabolism and behavior, the model provides a framework for examining cognitive changes in an obesity-related context. Researchers can investigate how disrupted hormonal signaling and neuroinflammation coincide with altered neural outcomes. These findings may help clarify links between obesity and neurological disease while supporting evaluation of potential interventions.