High-energy diets induce pathologies (e.g., metabolic syndrome, MS) in humans, and in animals used in experiments. Excess N intake creates certain disposal problems, whereas massive lipid intake (a ‘human’ discovery) lacks specific mechanisms to prevent this excess energy, resulting in unwanted fat accrual. However, fat alone is easily used as a substrate when energy and protein availability/intake are upkept. MS is also favored by palatable food. These changes are affected by sex-related differences and age, through largely unknown molecular/endocrine mechanisms. In aging men, lower testosterone enhances fat deposition, but in women, estrogen helps to limit body fat by increasing fat oxidation. Starches and other glucose sources have often been limited to make space in the diet for palatable fats and protein. There is a lack of molecular-based quantitative studies on what causes the MS-driven conversion of dietary glucose to fat but preserving dietary fat for triacylglycerol deposition, both related to altered insulin (and glucocorticoid) function. Testosterone and estradiol effects on the use of glucose for energy may provide additional clues regarding how to counteract inflammation in MS when using high-energy diets (largely fat) destabilizing insulin–glucocorticoid regulation. Nevertheless, it remains critical to quantitatively evaluate how much dietary glucose is needed to maintain energy homeostasis.

Dr. Xavier Remesar, professor of Nutrition & Food Science
Dr. Marià Alemany, emeritus professor of Biochemistry & Molecular Biology
Guest Editors

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• Glucose
• Lactate
• Metabolic syndrome
• Testosterone
• Estradiol High-energy diets
• Energy balance