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Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

Regulation of Metabolism

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Translocation of Proteins into the Mitochondria

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Related Experiment Video

Updated: Jul 9, 2026

The Use of the Patch-Clamp Technique to Study the Thermogenic Capacity of Mitochondria

The Use of the Patch-Clamp Technique to Study the Thermogenic Capacity of Mitochondria

Published on: May 3, 2021

Mitochondrial thermogenesis and obesity.

Ségolène Gambert¹, Daniel Ricquier

¹Biologie des transporteurs mitochondriaux et métabolisme, Université Paris Descartes, CNRS, Paris, France.

Current Opinion in Clinical Nutrition and Metabolic Care

|December 20, 2007

Summary

Mitochondria are key to thermogenesis and energy balance. Research into their role in fat oxidation and adaptive thermogenesis may offer new strategies for obesity and diet restriction.

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Determining Basal Energy Expenditure and the Capacity of Thermogenic Adipocytes to Expend Energy in Obese Mice

Published on: November 11, 2021

Area of Science:

Metabolism and Endocrinology
Mitochondrial Biology
Obesity Research

Background:

Thermogenesis, the process of heat production, is intrinsically linked to the oxidation of carbon molecules.
Mitochondria are central to cellular oxidation and heat generation, though energy recovery from oxidation is incomplete.
Understanding mitochondriogenesis and mitochondrial thermogenesis is crucial for advancing obesity research.

Purpose of the Study:

To review recent findings on thermogenesis, focusing on the role of mitochondria.
To explore the impact of mitochondrial function on energy partitioning and fat metabolism.
To identify potential research avenues for combating obesity and understanding adaptive thermogenesis.

Main Methods:

Review of recent scientific literature on thermogenesis, mitochondria, and obesity.
Analysis of studies investigating fat oxidation in skeletal muscle and adipose tissue.
Examination of the role of peroxisome proliferator-activated receptor gamma coactivators and thyroid hormones.

Main Results:

Prolonged food restriction unexpectedly decreases thermogenesis, limiting fat loss.
Fat oxidation in skeletal muscle is a viable strategy against fat accumulation.
Adipose depots can promote thermogenesis via mitochondrial uncoupling protein or other mechanisms.
Peroxisome proliferator-activated receptor gamma coactivators (alpha and beta) and thyroid hormones are key regulators of mitochondrial thermogenesis.
Brain mitochondria influence refeeding control post-starvation, highlighting their dual role in thermogenesis and energy partitioning.

Conclusions:

Investigating mechanisms that inhibit adaptive thermogenesis during diet restriction is essential.
The contribution of transcriptional coactivators to adipocyte plasticity warrants further research.
Adipocytes possess an underestimated capacity for fatty acid oxidation, beyond triglyceride storage.