The Interaction Between Metabolic Dysfunction and Hypothalamic Inflammation

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 395

Special Issue Editor


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Guest Editor
Department of Biochemistry, School of Biological Sciences, Federal University of Santa Catarina, Florianópolis, SC, Brazil
Interests: obesity; neuroinflammation; metabolism; metabolic disorders; neuropsy-chiatry disorders
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Special Issue Information

Dear Colleagues,

The regulation of energy homeostasis is a complex and highly coordinated process designed to maintain the stability of body energy stores over time. The hypothalamus serves as the primary center for regulating whole-body energy metabolism. It plays a crucial role in thermoregulation, satiety, sleep, sexual behavior, and emotional control. Hypothalamic neural cells respond to peripheral signals that regulate food intake, energy expenditure, and glucose and lipid metabolism in a homeostatic manner. Additionally, the hypothalamus integrates with limbic and cortical areas to coordinate hedonic responses to food.

Disruptions in the communication between the hypothalamus, other brain regions, and peripheral organs contribute to the development of chronic conditions, such as obesity, type 2 diabetes, and cardiovascular diseases. This Special Issue explores the role of the hypothalamus as a central regulator of whole-body energy metabolism. Key areas of focus include, but are not limited to, the molecular mechanisms underlying hypothalamic physiology and pathophysiology in regulating food intake, energy expenditure, and liver metabolism; the influence of microbiota and the gut–brain axis on energy homeostasis; obesity-induced neuroinflammation and dysregulated brain metabolism; and potential molecular targets for obesity treatment. Submissions addressing other relevant and emerging challenges in this field are also highly encouraged.

Dr. Joana M. Gaspar
Guest Editor

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Keywords

  • metabolic disorders
  • neuroinflammation
  • hypothalamus
  • energy homeostasis
  • feeding behavior
  • high-fat diets
  • obesity

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Published Papers (1 paper)

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Research

16 pages, 1558 KB  
Article
Chronic Caffeine Consumption Prevents Body Weight Gain and Glucose Intolerance in High-Fat Diet-Induced Obesity Mice Model
by Giuseppe Faraco, Natália F. Mendes, Luisa O. Schmitt, Tamires S. Stivanin, Elisa Gaspar, Nicolle Platt, Manuella P. Kaster and Joana M. Gaspar
Metabolites 2026, 16(6), 381; https://doi.org/10.3390/metabo16060381 - 31 May 2026
Viewed by 114
Abstract
Background/Objectives: Caffeine consumption has been reported to have beneficial effects in metabolic disorders; however, its effects on food intake are not fully elucidated. This study evaluated the impact of chronic caffeine consumption on weight gain, food intake, and metabolic parameters in C57BL/6 [...] Read more.
Background/Objectives: Caffeine consumption has been reported to have beneficial effects in metabolic disorders; however, its effects on food intake are not fully elucidated. This study evaluated the impact of chronic caffeine consumption on weight gain, food intake, and metabolic parameters in C57BL/6 male mice. Methods: Eight-week-old male mice (28 animals) were divided into four groups: control (chow diet), caffeine (chow diet + 1 g/L caffeine in drinking water), high-fat diet (HFD), and HFD + caffeine (HFD + 1 g/L caffeine in drinking water). Diets and caffeine were provided ad libitum for 8 weeks. Food and water intake were recorded weekly, and blood glucose was measured every 4 weeks. After 8 weeks of diet and caffeine exposure, metabolic tests were conducted, and tissues were collected for biochemical analysis. Results: HFD consumption for 8 weeks induced an increase in body weight and adiposity compared to the chow diet, without changes in food intake. Caffeine consumption prevented body weight gain and adiposity, although it increased food intake. Caffeine also improved glucose tolerance in the HFD mouse model, without changes in random blood glucose, triglyceride, or cholesterol levels. Analysis of hypothalamic neuropeptide (Agrp, NPY, Pomc, Cart), involved in the control of food intake, showed no differences in expression. There were also no changes observed in locomotion nor in anxiety-like behavior. Conclusions: In conclusion, chronic high-fat diet (HFD) exposure induced obesity characterized by increased body weight and adiposity without altering food intake. Chronic caffeine consumption counteracted HFD-induced weight gain and fat accumulation and improved glucose tolerance, despite increasing food intake. Importantly, caffeine consumption in the HFD group did not affect locomotor activity or anxiety-like behavior, suggesting that its metabolic effects are not driven by changes in general activity or emotional state. Overall, these findings indicate that chronic caffeine consumption improves metabolic homeostasis in HFD-fed mice. Full article
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