Regulation of energy intake and mechanisms of metabolic adaptation or maladaptation after caloric restriction
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Regulation of energy intake and mechanisms of metabolic adaptation or maladaptation after caloric restriction Roberto Vettor 1
&
Angelo Di Vincenzo 1 & Pietro Maffei 1 & Marco Rossato 1
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Despite their critical role in susceptibility to metabolic diseases such as obesity and type 2 diabetes, mechanisms regulating energy balance are extremely complex and far from being fully understood. Both central and peripheral feedback circuits are involved and, despite it was traditionally thought that the energy balance of an organism depends on the equality between calorie intake within the system and energy expenditure, the regulation of energy content in biological systems oversteps the classical physical laws of thermodynamics. The fine-tuned mechanism for body weight and energy storage regulation is aimed to preserve survival chances in response to the variations of energy availability, as expressed by the metabolic flexibility of this system adapting subjects to both starvation and overfeeding. However, these mechanisms can lose their flexibility, with consequent maladaptation to both increased energy intake and calorie restriction leading to the development of several metabolic disturbances. Keywords Energy intake . Calorie restriction . Metabolic adaptation . Adipocytes . Food intake
Abbreviations 5-HT serotonin α-MSH α-melanocyte-stimulating hormone AgRP agouti-related protein AMP adenosine monophosphate ATP adenosine triphosphate BAT brown adipose tissue BMI body mass index BW body weight CALERIE Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy CNS central nervous system CR caloric restriction CREB cAMP response element-binding protein DiRECT DIabetes REmission Clinical Trial
EE EI FFA FGF-21 GLP-1 LCD MC4R NPY PGC-1α POMC PPAR-α RCT REE VLCD WAT
energy expenditure energy intake free fatty acids fibroblast growth factor-21 glucagon-like peptide 1 low calorie diet melanocortin-4 receptor neuropeptide Y peroxisome proliferator-activated receptor gamma coactivator 1-α pro-opiomelanocortin peroxisome proliferator-activated receptor-α randomized controlled trial resting energy expenditure very low calorie diet white adipose tissue
1 Introduction * Roberto Vettor [email protected] 1
Department of Medicine – DIMED, University of Padova, Via Giustiniani 2, 35128 Padova, Italy
In a simplistic way, it was usually thought that the energy balance of a cell, an organ or an individual depends on the equality between entry and exit or between calories introduced within the system and energy expenditure, thinking that biological systems obey to the fundamental principles of thermodynamics. According to these principles, because energy
Rev Endocr Metab Disord
cannot be created or destroyed, energy input must be equal to energy output or, using an equation: energy in food consumed ¼ external work þ internal heat production þ =−stored energy In general this is plausible, although the complex organization of living be
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