Energy allocation between brain and body during ontogenetic development

Kubera, Britta; Bosy‐Westphal, Anja; Peters, Achim; Braun, Wiebke; Langemann, Dirk; Neugebohren, Stephanie; Heller, Martin; Müller, Manfred J.

doi:10.1002/ajhb.22439

Cited by 12 publications

(10 citation statements)

References 40 publications

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“…Energy allocation to peripheral organs (like skeletal muscle) is relatively higher during growth and adolescence. 59 As brain is the only organ, which does not lose weight with weight loss, 60 its position within whole-body energy allocation is unique. Comparing humans and apes the larger brain size of humans explains their greater EE.…”

Section: Energy Allocation To the Brain Controls Body Eementioning

confidence: 99%

From the past to future: from energy expenditure to energy intake to energy expenditure

Müller

Geisler

2016

Eur J Clin Nutr

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Although most recent research on energy balance focusses on energy intake (EI) there is still need to think about both sides of the energy balance. Current research on energy expenditure (EE) relates to metabolic adaptation to negative energy balance, mitochondrial metabolism associated with aging, obesity and type 2 diabetes mellitus, the role of EE in hunger and appetite control, non-shivering thermogenesis and brown adipose tissue activity, cellular bioenergetics as a target of obesity treatment and the evolutionary and ecological determinants of EE in humans and other primates. As far as regulation of energy balance is concerned there is recent evidence that EE rather than body weight is under tight control. Biologically, EE is maintained within a narrow physiological range. An EE-set point has been proposed as the width between the upper and lower boundaries of the individual EE range. Regulation of EE may fail in very obese patients with an EI above their upper boundary and after drastic weight loss when patients may go far below their lower EE boundary and thus are loosing control. In population studies, fat-free mass (FFM) and its composition (that is, the proportion of high to low metabolic rate organs) are major determinants of EE. It is tempting to speculate that tight biologic control of EE is related to brain energy need, which is preserved at the cost of peripheral metabolism. There is a moderate heritability of EE, which is independent of the heritability of FFM. In future, metabolic phenotyping should focus on the EE–FFM relationship rather than on EE-values alone.

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Section: Energy Allocation To the Brain Controls Body Eementioning

confidence: 99%

From the past to future: from energy expenditure to energy intake to energy expenditure

Müller

Geisler

2016

Eur J Clin Nutr

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“…Thus, updating the probabilities of the competing hypothesis with the help of Krieger's data gave a huge boost to the brain-pull hypothesis. Adding further evidence from experiments using state-of-the-art technology, including magnet resonance imaging and spectroscopy (Peters et al, 2011;Kubera et al, 2013;Oltmanns et al, 2008;Goodman et al, 1984;Muhlau et al, 2007) and positron-emission-tomography (Kuzawa et al, 2014), more and more increased the likelihood of the brain-pull hypothesis being true. Now, that the conventional view advocating the null hypothesis has become increasingly unlikely, it seems promising to look at the 'obesity paradox' observations in the light of brain-pull mechanisms.…”

Section: Brain Energy 'Supply and Demand'mentioning

confidence: 96%

Stress habituation, body shape and cardiovascular mortality

Peters

McEwen

2015

Neuroscience & Biobehavioral Reviews

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117

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High cardiovascular mortality is well documented in lean phenotypes exhibiting visceral fat accumulation. In contrast, corpulent phenotypes with predominantly subcutaneous fat accumulation display a surprisingly low mortality. The term 'obesity paradox' reflects the difficulty in understanding the biological mechanisms underlying these clinical observations. The allostatic load model of chronic stress focuses on glucocorticoid dysregulation as part of a 'network of allostasis' involving autonomic, endocrine, metabolic, and immune mediators. Here, we expand upon the energetic demands of the brain and show that 'habituators' and 'non-habituators' develop divergent patterns of fat distribution. Central to this process is the recurrent rise in the cerebral energy need (arousal) that non-habituators experience during chronic stress. These neuroenergetic alterations promote visceral fat accumulation, subcutaneous fat loss, and atherogenesis with subsequent cardiovascular events. Habituators are more or less protected against such cardiovascular complications, but there is a metabolic trade-off that we shall discuss in the present paper.

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“…Although an important precursor to type 2 diabetes, peripheral insulin resistance is also effective at shunting scarce glucose to high-demand tissues or organs, such as to the fetus during the mild diabetes of pregnancy (58), or to the brain during the insulin-resistance triggered by stress (59). Changes in insulin secretion are believed to help coordinate glucose delivery to the brain as brain size and energy requirements change during development (60,61). The present finding that the brain's requirement for glucose peaks after weaning, at an age when body fat stores are minimal (18), points to strong selection on physiologic mechanisms to redirect glucose delivery to the brain during nutritional stress.…”

Section: Discussionmentioning

confidence: 99%

Metabolic costs and evolutionary implications of human brain development

Kuzawa

Chugani

Grossman

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

433

393

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The high energetic costs of human brain development have been hypothesized to explain distinctive human traits, including exceptionally slow and protracted preadult growth. Although widely assumed to constrain life-history evolution, the metabolic requirements of the growing human brain are unknown. We combined previously collected PET and MRI data to calculate the human brain's glucose use from birth to adulthood, which we compare with body growth rate. We evaluate the strength of brain-body metabolic trade-offs using the ratios of brain glucose uptake to the body's resting metabolic rate (RMR) and daily energy requirements (DER) expressed in glucose-gram equivalents (glucose rmr% and glucose der% ). We find that glucose rmr% and glucose der% do not peak at birth (52.5% and 59.8% of RMR, or 35.4% and 38.7% of DER, for males and females, respectively), when relative brain size is largest, but rather in childhood (66.3% and 65.0% of RMR and 43.3% and 43.8% of DER). Body-weight growth (dw/dt) and both glucose rmr% and glucose der% are strongly, inversely related: soon after birth, increases in brain glucose demand are accompanied by proportionate decreases in dw/dt. Ages of peak brain glucose demand and lowest dw/dt co-occur and subsequent developmental declines in brain metabolism are matched by proportionate increases in dw/dt until puberty. The finding that human brain glucose demands peak during childhood, and evidence that brain metabolism and body growth rate covary inversely across development, support the hypothesis that the high costs of human brain development require compensatory slowing of body growth rate.neuroimaging | diabetes | human evolution | neuronal plasticity | anthropology A prolonged period of childhood and juvenile growth is a defining feature of human life history (1-3). Compared with other great apes, human offspring are weaned early, leading to an extended period of dependence on procured resources rather than breast milk (1, 4). Although this unique human reproductive pattern is viewed as shortening the interbirth interval and thus increasing fertility (5, 6), what is less clear is why humans also grow so slowly during childhood. Although most primates grow slower than other mammals (7), human childhood and juvenile growth stand out as unusually slow even by primate and great ape standards, during which it proceeds at a pace more typical of reptiles than of mammals (8, 9). In humans, a sizeable percentage of preadult growth is deferred until the pubertal growth spurt, when growth rate markedly increases and adult size is achieved (1).Many hypotheses have been proposed to explain this slow and prolonged preadult life-stage, with most pointing to the extra time and energy required for human learning and brain development (5, 10-12). It has long been assumed that human cultural practices are sufficiently complex that they take many years to learn, which could have selected for a slowing down and extension of preadult development (13). A recent variant of this idea notes the importance of ...

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Energy allocation between brain and body during ontogenetic development

Cited by 12 publications

References 40 publications

From the past to future: from energy expenditure to energy intake to energy expenditure

From the past to future: from energy expenditure to energy intake to energy expenditure

Stress habituation, body shape and cardiovascular mortality

Metabolic costs and evolutionary implications of human brain development

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