Catch-up Fat Research Articles

The habitual degree of weight loss might be associated with specific fat and protein intakes during a period of weight maintenance in athletes used to weight variations: preliminary results from the WAVE study

Weight variations are common in sporting life, with important inter-individual variability in the degree of an athlete's habitual weight loss. As a part of the WAVE study (NCT04107545), the main objective of this preliminary study was to determine whether the habitual degree of weight loss was associated with anthropometric, body composition, nutritional or psychometric profiles during a period of weight maintenance in athletes accustomed to weight variations. We hypothesized that athletes accustomed to a higher habitual degree of weight loss may have a higher body weight and body fat mass, and may present a more controlled diet regimen and cognitive restriction than athletes with a lower habitual degree of weight loss. During a period of weight maintenance, 62 athletes (24.0 ± 5.3 years; 26 women) completed anthropometry and body composition measurements, a 48-hours food diary and self-reported questionnaires to determine their weight variation practice, nutritional profile and mood state. Athletes were stratified within inter- and intra-quartile groups according to their habitual degree of weight loss. Athletes with a higher habitual degree of weight loss were those who consumed more protein (P < .001) and less fat (P = .01) as a proportion of total energy compared with those losing less weight, without any difference in body composition between the groups. The rapid weight loss score was significantly higher in individuals losing more weight (P < .001) and no difference was observed for the mood state profile. The present results suggest a potential control of nutritional regulation during a period of weight maintenance in order to spare fat-free mass and favor fat mass loss in athletes who are routinely losing more weight. Fat-free mass may be the main nutritional driver due to low body fat mass in athletes, which may limit the “catch-up fat” phenomenon commonly observed in nonathletic population.

Peripheral thyroid hormone deiodination: Entry points to elucidate mechanisms of metabolic adaptation during weight regain.

The concept of dual-adaptive thermogenesis underlying metabolic adaptation to prolonged energy deficit posits that there are two control systems that govern energy sparing: a rapid-reacting system to energy deficit and a slow-reacting system to fat store depletion. The latter control system, referred to as the "adipose-specific" control of thermogenesis, contributes to accelerating fat store replenishment (catch-up fat) during weight regain. The case is put forward here that, whereas adaptive thermogenesis during weight loss results primarily from central suppression of the sympathetic nervous system and hypothalamic-pituitary-thyroid axis, during weight regain it operates primarily through peripheral tissue resistance to the actions of this neurohormonal network. Emerging evidence that altered deiodination of thyroid hormones within the skeletal muscle and liver is a key determinant of such peripheral resistance therefore offers entry points toward elucidating the molecular mechanisms that underlie the adipose-specific control of thermogenesis and unraveling tissue-specific targets to counter obesity recidivism.

Catch‐up fat in male adults induces low testosterone and consequently promotes metabolic abnormalities and cognitive impairment

Catch-up fat in adults (CUFA) caused by rapid nutrition promotion after undernutrition plays an important role in the epidemic of insulin resistance (IR)-related diseases in developing societies. Insulin resistance is considered to be closely associated with reduced testosterone levels and cognitive function. However, the effects of CUFA on testosterone levels and cognitive function are unclear in males. To investigate the changes in testosterone levels and cognitive function in CUFA in male humans and rats, and explore their probable relationship and mechanisms in rats. The blood testosterone levels, fasting glucose, and blood insulin (FINS) were measured in subpopulation 1 (27 CUFA individuals, 61 controls without CUFA) aged 40-50 years to show the characteristics of sex hormone levels and the metabolic status in CUFA men. Cognitive Flexibility Inventory was conducted in subpopulation 2 (54 CUFA individuals, 214 controls) over 20 years to investigate the associations between sex hormone levels, cognitive function, and CUFA. Male rats (n = 27) were randomly allocated to the NC group (normal chow controls), RN group (CUFA, refeeding after caloric restriction), and RT group (RN with testosterone intramuscular injected while refeeding). The blood testosterone levels, intraperitoneal insulin tolerance test (IPITT), and FINS were measured, and the attentional set-shifting task test (ASST) for the assessment of cognitive function was performed in these animals. Insulin signaling pathway, N-methyl-d-aspartate receptors subtype 2A (NR2A) and 2B (NR2B) expression levels were determined in the rat cerebral cortex. The total testosterone levels decreased (medium [inter-quartile ranges], 13.43 [9.87-18.96] vs. 15.58 [13.37-24.96], p = 0.036), and HOMA-IR (Homeostatic Model Assessment for Insulin Resistance) elevated (1.61 [1.08-2.33] vs. 1.24 [0.87-1.87], P = 0.037) in CUFA men in subpopulation 1. Additionally, cognitive impairment was observed in CUFA men in subpopulation 2. Moreover, our results indicated decreases in total and free testosterone levels, elevations in visceral lipid accumulation, FINS, HOMA-IR, blood glucose, and the area under the curve after IPITT, increases in the number of trials required to achieve the criterion of the first reversal of discrimination (R1) in ASST, and downregulation of IRS-1 mRNA expression, AKT phosphorylation, and the NR2A and NR2B expression in brain tissue in male CUFA rats. Notably, testosterone supplementation improved visceral lipid accumulation and IR-related metabolic disorders, cognitive dysfunction, decreases in IRS-1 mRNA expression, Akt phosphorylation, and NR2A and NR2B expression in brain tissue in male CUFA rodents. CUFA was characterized by reduced testosterone levels, metabolic abnormalities, and cognitive dysfunction in males, and testosterone supplementation attenuated these changes, as well as the alteration in insulin signaling and NR2A and NR2B expression in male CUFA rodents. Herein, we tentatively put forward that CUFA in males induces low testosterone, consequently promoting metabolic abnormalities and cognitive impairment probably mediated by defects in insulin signaling and NR2A, NR2B pathway in brain tissue.

Adaptive Thermogenesis Driving Catch-Up Fat Is Associated With Increased Muscle Type 3 and Decreased Hepatic Type 1 Iodothyronine Deiodinase Activities: A Functional and Proteomic Study.

Refeeding after caloric restriction induces weight regain and a disproportionate recovering of fat mass rather than lean mass (catch-up fat) that, in humans, associates with higher risks to develop chronic dysmetabolism. Studies in a well-established rat model of semistarvation-refeeding have reported that catch-up fat associates with hyperinsulinemia, glucose redistribution from skeletal muscle to white adipose tissue and suppressed adaptive thermogenesis sustaining a high efficiency for fat deposition. The skeletal muscle of catch-up fat animals exhibits reduced insulin-stimulated glucose utilization, mitochondrial dysfunction, delayed in vivo contraction-relaxation kinetics, increased proportion of slow fibers and altered local thyroid hormone metabolism, with suggestions of a role for iodothyronine deiodinases. To obtain novel insights into the skeletal muscle response during catch-up fat in this rat model, the functional proteomes of tibialis anterior and soleus muscles, harvested after 2 weeks of caloric restriction and 1 week of refeeding, were studied. Furthermore, to assess the implication of thyroid hormone metabolism in catch-up fat, circulatory thyroid hormones as well as liver type 1 (D1) and liver and skeletal muscle type 3 (D3) iodothyronine deiodinase activities were evaluated. The proteomic profiling of both skeletal muscles indicated catch-up fat-induced alterations, reflecting metabolic and contractile adjustments in soleus muscle and changes in glucose utilization and oxidative stress in tibialis anterior muscle. In response to caloric restriction, D3 activity increased in both liver and skeletal muscle, and persisted only in skeletal muscle upon refeeding. In parallel, liver D1 activity decreased during caloric restriction, and persisted during catch-up fat at a time-point when circulating levels of T4, T3 and rT3 were all restored to those of controls. Thus, during catch-up fat, a local hypothyroidism may occur in liver and skeletal muscle despite systemic euthyroidism. The resulting reduced tissue thyroid hormone bioavailability, likely D1- and D3-dependent in liver and skeletal muscle, respectively, may be part of the adaptive thermogenesis sustaining catch-up fat. These results open new perspectives in understanding the metabolic processes associated with the high efficiency of body fat recovery after caloric restriction, revealing new implications for iodothyronine deiodinases as putative biological brakes contributing in suppressed thermogenesis driving catch-up fat during weight regain.

Dietary Complex and Slow Digestive Carbohydrates Prevent Fat Deposits During Catch-Up Growth in Rats.

A nutritional growth retardation study, which closely resembles the nutritional observations in children who consumed insufficient total energy to maintain normal growth, was conducted. In this study, a nutritional stress in weanling rats placed on restricted balanced diet for 4 weeks is produced, followed by a food recovery period of 4 weeks using two enriched diets that differ mainly in the slow (SDC) or fast (RDC) digestibility and complexity of their carbohydrates. After re-feeding with the RDC diet, animals showed the negative effects of an early caloric restriction: an increase in adiposity combined with poorer muscle performance, insulin resistance and, metabolic inflexibility. These effects were avoided by the SDC diet, as was evidenced by a lower adiposity associated with a decrease in fatty acid synthase expression in adipose tissue. The improved muscle performance of the SDC group was based on an increase in myocyte enhancer factor 2D (MEF2D) and creatine kinase as markers of muscle differentiation as well as better insulin sensitivity, enhanced glucose uptake, and increased metabolic flexibility. In the liver, the SDC diet promoted glycogen storage and decreased fatty acid synthesis. Therefore, the SDC diet prevents the catch-up fat phenotype through synergistic metabolic adaptations in adipose tissue, muscle, and liver. These coordinated adaptations lead to better muscle performance and a decrease in the fat/lean ratio in animals, which could prevent long-term negative metabolic alterations such as obesity, insulin resistance, dyslipidemia, and liver fat deposits later in life.

Why and How Imprinted Genes Drive Fetal Programming.

Imprinted genes mediate fetal and childhood growth and development, and early growth patterns drive fetal programming effects. However, predictions and evidence from the kinship theory of imprinting have yet to be directly integrated with data on fetal programming and risks of metabolic disease. I first define paternal-gene and maternal-gene optima with regard to early human growth and development. Next, I review salient evidence with regard to imprinted gene effects on birth weight, body composition, trajectories of feeding and growth, and timing of developmental stages, to evaluate why and how imprinted gene expression influences risks of metabolic disease in later life. I find that metabolic disease risks derive primarily from maternal gene biases that lead to reduced placental efficacy, low birth weight, low relative muscle mass, high relative white fat, increased abdominal adiposity, reduced pancreatic β-cell mass that promotes insulin resistance, reduced appetite and infant sucking efficacy, catch-up fat deposition from family foods after weaning, and early puberty. Paternal gene biases, by contrast, may contribute to metabolic disease via lower rates of brown fat thermiogenesis, and through favoring more rapid postnatal catch-up growth after intrauterine growth restriction from environmental causes. These disease risks can be alleviated through dietary and pharmacological alterations that selectively target imprinted gene expression and relevant metabolic pathways. The kinship theory of imprinting, and mother-offspring conflict more generally, provide a clear predictive framework for guiding future research on fetal programming and metabolic disease.

Low 24-hour core body temperature as a thrifty metabolic trait driving catch-up fat during weight regain after caloric restriction.

The recovery of body weight after substantial weight loss or growth retardation is often characterized by a disproportionately higher rate of fat mass vs. lean mass recovery, with this phenomenon of "preferential catch-up fat" being contributed by energy conservation (thrifty) metabolism. To test the hypothesis that a low core body temperature (Tc) constitutes a thrifty metabolic trait underlying the high metabolic efficiency driving catch-up fat, the Anipill system, with telemetry capsules implanted in the peritoneal cavity, was used for continuous monitoring of Tc for several weeks in a validated rat model of semistarvation-refeeding in which catch-up fat is driven solely by suppressed thermogenesis. In animals housed at 22°C, 24-h Tc was reduced in response to semistarvation (-0.77°C, P < 0.001) and remained significantly lower than in control animals during the catch-up fat phase of refeeding (-0.27°C on average, P < 0.001), the lower Tc during refeeding being more pronounced during the light phase than during the dark phase of the 24-h cycle (-0.30°C vs. -0.23°C, P < 0.01) and with no between-group differences in locomotor activity. A lower 24-h Tc in animals showing catch-up fat was also observed when the housing temperature was raised to 29°C (i.e., at thermoneutrality). The reduced energy cost of homeothermy in response to caloric restriction persists during weight recovery and constitutes a thrifty metabolic trait that contributes to the high metabolic efficiency that underlies the rapid restoration of the body's fat stores during weight regain, with implications for obesity relapse after therapeutic slimming and the pathophysiology of catch-up growth.

126-OR: Fat Catch-Up Growth in Early Infancy and Cardiometabolic Outcomes at 5 Years of Age

Introduction: The role of infant fat growth in childhood obesity and adult type 2 diabetes is not clear. We have previously used latent class analysis (LCA) to identify four distinct fat mass (FM) growth patterns in early infancy. Here we examine their associations with adiposity and cardiometabolic outcomes at 5 years (y) of age. Methods: Air Displacement Plethysmography (ADP) was used to repeatedly measure FM from 0-6 months of age in a cohort of 314 healthy urban-living Ethiopian infants and LCA was used to identify FM growth patterns (catch-up, accelerated, average and delayed) (Figure 1). At 5y of age, cardiometabolic outcomes were obtained from ADP and blood samples. Multiple linear regression was used to examine associations between infant FM growth patterns and cardiometabolic outcomes at 5y, adjusted for gender, birthweight, breastfeeding, maternal age and education and SES. Results: Overall mean (SD) BMI at 5y was 14.98 (1.19) kg/m2. Compared to children with an “average fat” growth pattern, children with a "catch-up fat" pattern had significantly higher BMI (0.79 kg/m2 [95% CI, 0.04; 1.54]) and FMI (0.69 kg/m2 [95% CI, 0.06; 1.37]), but not FFMI (0.05 kg/m2 [-0.51; 0.62]) at 5y of age (Figure 1). There were no differences in any other cardiometabolic outcomes. Conclusions: Fat catch-up growth in early infancy was associated with a higher BMI in childhood, which was almost entirely fueled by increased adipose tissue. Disclosure G.S. Andersen: Stock/Shareholder; Self; Novo Nordisk Inc. R. Wibaek: None. B. Admassu: None. D. Vistisen: Stock/Shareholder; Self; Novo Nordisk A/S. M.E. Jørgensen: Research Support; Self; Amgen Inc., AstraZeneca, Danish Diabetes Association, Sanofi-Aventis. Stock/Shareholder; Self; Novo Nordisk A/S. K.F. Michaelsen: None. J.C. Wells: None. H. Friis: Research Support; Self; Arla Food for Health. Funding Danish Council for Strategic Research; Danida (104.Dan.8-1207); Danish Diabetes Academy; Innovation Fund, Denmark

Reduced Skeletal Muscle Protein Turnover and Thyroid Hormone Metabolism in Adaptive Thermogenesis That Facilitates Body Fat Recovery During Weight Regain.

Objective: The recovery of body composition after weight loss is characterized by an accelerated rate of fat recovery (preferential catch-up fat) resulting partly from an adaptive suppression of thermogenesis. Although the skeletal muscle has been implicated as an effector site for such thrifty (energy conservation) metabolism driving catch-up fat, the underlying mechanisms remain to be elucidated. We test here the hypothesis that this thrifty metabolism driving catch-up fat could reside in a reduced rate of protein turnover (an energetically costly “futile” cycle) and in altered local thyroid hormone metabolism in skeletal muscle.Methods: Using a validated rat model of semistarvation-refeeding in which catch-up fat is driven solely by suppressed thermogenesis, we measured after 1 week of refeeding in refed and control animals the following: (i) in-vivo rates of protein synthesis in hindlimb skeletal muscles using the flooding dose technique of 13C-labeled valine incorporation in muscle protein, (ii) ex-vivo muscle assay of net formation of thyroid hormone tri-iodothyronine (T3) from precursor hormone thyroxine (T4), and (iii) protein expression of skeletal muscle deiodinases (type 1, 2, and 3).Results: We show that after 1 week of calorie-controlled refeeding, the fractional protein synthesis rate was lower in skeletal muscles of refed animals than in controls (by 30–35%, p < 0.01) despite no between-group differences in the rate of skeletal muscle growth or whole-body protein deposition—thereby underscoring concomitant reductions in both protein synthesis and protein degradation rates in skeletal muscles of refed animals compared to controls. These differences in skeletal muscle protein turnover during catch-up fat were found to be independent of muscle type and fiber composition, and were associated with a slower net formation of muscle T3 from precursor hormone T4, together with increases in muscle protein expression of deiodinases which convert T4 and T3 to inactive forms.Conclusions: These results suggest that diminished skeletal muscle protein turnover, together with altered local muscle metabolism of thyroid hormones leading to diminished intracellular T3 availability, are features of the thrifty metabolism that drives the rapid restoration of the fat reserves during weight regain after caloric restriction.

Body Composition Growth Patterns in Early Infancy: A Latent Class Trajectory Analysis of the Ethiopian iABC Birth Cohort.

The objective of this study was to identify subgroups with distinct fat and fat-free growth patterns in the first 6 months of life and describe predictors of these different patterns. A total of 510 apparently healthy Ethiopian infants were followed from birth to 6 months of age. Each infant had at least three and up to six repeated measurements of fat and fat-free mass using air-displacement plethysmography. Latent class trajectory analyses were used to categorize infants in groups with distinct body composition patterns. Four distinct fat mass and two fat-free mass growth patterns were identified. Of the infants measured, 5% presented a delayed fat growth pattern and 3% presented a catch-up fat growth pattern involving low birth weight but a significant fat growth velocity from 2.5 to 6 months. A large class had a high fat level at birth and an accelerated fat growth pattern in early infancy. Fat-free growth was represented by two distinct classes with less variability. Catch-up growth was primarily seen in fat mass. We identified distinct patterns of delayed, catch-up, and accelerated fat growth in early infancy. This variability is not detected in regular anthropometric assessment and could be a mechanism linking early growth with later obesity and cardiometabolic risk.

Intermittent hypoxia suppression of growth hormone and insulin-like growth factor-I in the neonatal rat liver

ObjectivesExtremely low gestational age neonates with chronic lung disease requiring oxygen therapy frequently experience fluctuations in arterial oxygen saturation or intermittent hypoxia (IH). These infants are at risk for multi-organ developmental delay, reduced growth, and short stature. The growth hormone (GH)/insulin-like growth factor-I (IGF-1) system, an important hormonal regulator of lipid and carbohydrate metabolism, promotes neonatal growth and development. We tested the hypothesis that increasing episodes of IH delay neonatal growth by influencing the GH/IGF-I axis. DesignNewborn rats were exposed to 2, 4, 6, 8, 10, or 12 hypoxic episodes (12% O2) during hyperoxia (50% O2) from P0-P7, P0-P14 (IH), or allowed to recover from P7-P21 or P14-P21 (IHR) in room air (RA). RA littermates at P7, P14, and P21 served as RA controls; and groups exposed to hyperoxia only (50% O2) served as zero IH controls. Histopathology of the liver; hepatic levels of GH, GHBP, IGF-I, IGFBP-3, and leptin; and immunoreactivities of GH, GHR, IGF-I and IGF-IR were determined. ResultsPathological findings of the liver, including cellular swelling, steatosis, necrosis and focal sinusoid congestion were seen in IH, and were particularly severe in the P7 animals. Hepatic GH levels were significantly suppressed in the IH groups exposed to 6–12 hypoxic episodes per day and were not normalized during IHR. Deficits in the GH levels were associated with reduced body length and increase body weight during IHR suggesting increased adiposity and catchup fat. Catchup fat was also associated with elevations in GHBP, IGF-I, leptin. ConclusionsIH significantly impairs hepatic GH/IGF-1 signaling during the first few weeks of life, which is likely responsible for hepatic GH resistance, increased body fat, and hepatic steatosis. These hormonal perturbations may contribute to long-term organ and body growth impairment, and metabolic dysfunction in preterm infants experiencing frequent IH and/or apneic episodes.

Tannerella forsythia and coating color on the tongue dorsum, and fatty food liking associate with fat accumulation and insulin resistance in adult catch-up fat.

We aimed to determine the alteration of Tannerella forsythia and coating color on the dorsal tongue, and fatty food liking in catch-up fat in adult (CUFA), as well as the probable associations between fat accumulation, insulin resistance (IR) and these changes. T. forsythia on the tongue dorsum, fatty food liking, fat accumulation and insulin sensitivity were investigated in CUFA humans and rats, and tongue-coating color was observed in CUFA individuals. We further determined the changes of fatty food liking, fat accumulation and IR in T. forsythia-infected rodents by oral lavage. Increases in fat accumulation, IR, percentage of subjects with yellow tongue coating and that with T. forsythia detected were observed in CUFA individuals. Additionally, the fat ranking scores were significantly lower and the hedonic ratings of low-fat options of sampled food were lower, while the ratings of high-fat options were remarkably higher in CUFA subjects. Additionally, T. forsythia level elevated in CUFA rats, and fatty food liking, fat accumulation and IR increased in CUFA and T. forsythia-infected animals, with the increases in T. forsythia infection and fatty food liking preceding the occurrence of fat accumulation and IR. T. forsythia and yellow coating on the dorsal tongue and fatty food liking associate fat accumulation and IR in CUFA. Moreover, we tentatively put forward that T. forsythia, which is very important in yellow tongue-coating microbiota, and its consequent increases in fatty food liking, might be crucial in the development of fat accumulation and IR in CUFA.

Editorial: Hormonal and Neuroendocrine Regulation of Energy Balance.

Editorial: Hormonal and Neuroendocrine Regulation of Energy Balance.

Catch-up growth and catch-up fat in children born small for gestational age.

Infants born small for gestational age (SGA) are at increased risk of perinatal morbidity, persistent short stature, and metabolic alterations in later life. Recent studies have focused on the association between birth weight (BW) and later body composition. Some reports suggest that fetal nutrition, as reflected by BW, may have an inverse programing effect on abdominal adiposity later in life. This inverse association between BW and abdominal adiposity in adults may contribute to insulin resistance. Rapid weight gain during infancy in SGA children seemed to be associated with increased fat mass rather than lean mass. Early catch-up growth after SGA birth rather than SGA itself has been noted as a cardiovascular risk factor in later life. Children who are born SGA also have a predisposition to accumulation of fat mass, particularly intra-abdominal fat. It is not yet clear whether this predisposition is due to low BW itself, rapid postnatal catch-up growth, or a combination of both. In this report, we review the published literature on central fat accumulation and metabolic consequences of being SGA, as well as the currently popular research area of SGA, including growth aspects.

Caloric restriction induces energy-sparing alterations in skeletal muscle contraction, fiber composition and local thyroid hormone metabolism that persist during catch-up fat upon refeeding.

Weight regain after caloric restriction results in accelerated fat storage in adipose tissue. This catch-up fat phenomenon is postulated to result partly from suppressed skeletal muscle thermogenesis, but the underlying mechanisms are elusive. We investigated whether the reduced rate of skeletal muscle contraction-relaxation cycle that occurs after caloric restriction persists during weight recovery and could contribute to catch-up fat. Using a rat model of semistarvation-refeeding, in which fat recovery is driven by suppressed thermogenesis, we show that contraction and relaxation of leg muscles are slower after both semistarvation and refeeding. These effects are associated with (i) higher expression of muscle deiodinase type 3 (DIO3), which inactivates tri-iodothyronine (T3), and lower expression of T3-activating enzyme, deiodinase type 2 (DIO2), (ii) slower net formation of T3 from its T4 precursor in muscles, and (iii) accumulation of slow fibers at the expense of fast fibers. These semistarvation-induced changes persisted during recovery and correlated with impaired expression of transcription factors involved in slow-twitch muscle development. We conclude that diminished muscle thermogenesis following caloric restriction results from reduced muscle T3 levels, alteration in muscle-specific transcription factors, and fast-to-slow fiber shift causing slower contractility. These energy-sparing effects persist during weight recovery and contribute to catch-up fat.

How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery.

Whether dieting makes people fatter has been a subject of considerable controversy over the past 30 years. More recent analysis of several prospective studies suggest, however, that it is dieting to lose weight in people who are in the healthy normal range of body weight, rather than in those who are overweight or obese, that most strongly and consistently predict future weight gain. This paper analyses the ongoing arguments in the debate about whether repeated dieting to lose weight in normal-weight people represents unsuccessful attempts to counter genetic and familial predispositions to obesity, a psychosocial reaction to the fear of fatness or that dieting per se confers risks for fatness and hence a contributing factor to the obesity epidemic. In addressing the biological plausibility that dieting predisposes the lean (rather than the overweight or obese) to regaining more body fat than what had been lost (i.e. fat overshooting), it integrates the results derived from the re-analysis of body composition data on fat mass and fat-free mass (FFM) losses and recoveries from human studies of experimental energy restriction and refeeding. These suggest that feedback signals from the depletion of both fat mass (i.e. adipostats) and FFM (i.e. proteinstats) contribute to weight regain through the modulation of energy intake and adaptive thermogenesis, and that a faster rate of fat recovery relative to FFM recovery (i.e. preferential catch-up fat) is a central outcome of body composition autoregulation in lean individuals. Such a temporal desynchronization in the restoration of the body's fat vs. FFM results in a state of hyperphagia that persists beyond complete recovery of fat mass and interestingly until FFM is fully recovered. However, as this completion of FFM recovery is also accompanied by fat deposition, excess fat accumulates. In other words, fat overshooting is a prerequisite to allow complete recovery of FFM. This confers biological plausibility for post-dieting fat overshooting - which through repeated dieting and weight cycling would increase the risks for trajectories from leanness to fatness. Given the increasing prevalence of dieting in normal-weight female and male among young adults, adolescents and even children who perceive themselves as too fat (due to media, family and societal pressures), together with the high prevalence of dieting for optimizing performance among athletes in weight-sensitive sports, the notion that dieting and weight cycling may be predisposing a substantial proportion of the population to weight gain and obesity deserves greater scientific scrutiny.

Early postnatal alteration of body composition in preterm and small-for-gestational-age infants: implications of catch-up fat

The concept of the developmental origins of health and disease is based on studies by Barker et al. They proposed a hypothesis that undernutrition in utero permanently changes the body's structure, function, and metabolism in ways that lead to atherosclerosis and insulin resistance in later life. In addition, profound effects on the extent of body fatness and insulin sensitivity are demonstrated, if there is a "mismatch" between prenatal and postnatal environments. In previous studies, undernutrition in utero has been evaluated simply by birth weight itself or birth weight for gestational age, and the degree of mismatch has been estimated by postnatal rapid weight gain. Recently, we investigated subcutaneous fat accumulation in small-for-gestational-age infants and found that a rapid catch-up in skinfold thickness developed prior to the body weight catch-up. Furthermore, insulin-like growth factor-I and lipoprotein lipase mass concentrations also demonstrate rapid increase during the neonatal period with fat accumulation. Investigating the precise mechanisms of developmental origins of health and disease including mediating metabolic and hormonal factors may provide a new approach to prevent atherosclerosis and insulin resistance. Better management of undernutrition during gestation and neonatal growth during the early postnatal period is an important theme for future health.

Effect of liraglutide on catch-up fat in high-fat diet-induced catch-up growth rat model

Objective To investigate whether liraglutide treatment can prevent catch-up fat in high-fat dietinduced catch-up growth rats,and to discuss the possible underlying mechanisms.Methods Sixty-four SpragueDawley rats were stratified into 4 groups:normal control group,catch-up growth (CUG) group,catch-up growth with liraglutide treatment (CUGL) group,and catch-up growth with liraglutide plus exendin (9-39) treatment (CUGLE) group.All the catch-up growth animals underwent a4 week high-fat diet re-feeding phase after a4 week food restriction phase.Body weight and food intake were measured every day.At the end of food restriction and re-feeding,body composition was measured via Dual energy X-ray absorptiometry.After the rats were sacrificed,body fat distribution and plasma lipid levels were determined.Results By the end of catch-up growth,body weight,energy intake,Lee' s index,fat body mass,visceral adipose tissue/body weight,subcutaneous adipose tissue/body weight,triglyceride,free fatty acid,low density lipoprotein-cholesterol levels were lower in CUGL rats compared with CUG rats (all P＜0.01).There were no significant differences in energy intake,body composition,fat body mass,and blood lipid levels between CUGLE rats and CUG rats,while the weight of CUGLE rats was significantly lower than CUG ones.Conclusions Liraglutide infusion protects rats with high-fat diet induced catch-up growth from catch-up fat mainly via a glucagon-like peptide-1 receptor dependent manner. Key words: Catch-up growth; High-fat diet; Glucagon-like peptide-1 ; Catch-up fat

Growth and body composition changes in late preterm infants in the first months of life

The aim of this study was to compare growth and body composition of late preterm infants to that of extremely preterm and full-term infants. Observational longitudinal study. Forty-nine late preterm infants and 63 extremely preterm infants were included in the study. Forty healthy, full-term, breast-fed infants were enrolled as a reference group. Anthropometric parameters and body composition by an air displacement plethysmography system were assessed at 36th week, at term, at 1 and 3 months of corrected age in all groups. Late preterm infants were also assessed on the fifth day of life. Late preterm infants showed higher weight, length and head circumference values than those of very low birth weight infants but lower fat mass values on the fifth day of life and at 36th week of corrected age. However, at 3 months of corrected age, percentage of fat mass in late preterm infants reached values comparable with those of very low birth weight infants, probably because of the fast catch-up fat recorded between the fifth day of life and term corrected age. Moreover, percentage of fat mass in the first month of corrected age in preterm infants was higher as compared with full-term infants. This difference was no longer found at 3 months of corrected age. Further studies are needed to investigate whether this rapid increase in fat mass may modulate the risk of chronic diseases.

Higher body fatness in intrauterine growth retarded juvenile pigs is associated with lower fat and higher carbohydrate oxidation during ad libitum and restricted feeding

Purpose A thrifty energy metabolism has been suggested in intrauterine growth restricted (IUGR) offspring. We characterized energy metabolism and substrate oxidation patterns in IUGR pigs in response to food restriction (FR) and refeeding (RFD).MethodsFemale pigs with low (L; 1.1 kg; n = 20) or normal birth weight (N; 1.5 kg; n = 24) were fed ad libitum after weaning. Half of L and N pigs were food restricted (R; LR, NR) from days 80 to 100 (57 % of ad libitum) and refeed from days 101 to 131, while the remaining pigs were fed ad libitum (control, C). Using indirect calorimetry, carbohydrate and fat oxidation (COX, FOX), energy expenditure (EE) and balance (EB), resting metabolic rate (RMR) [all related to kg body weight0.62 (BW)] and RQ were determined at 4 days before (day 76) and after (day 83) beginning of FR, 4 days before (day 97) and after (day 104) end of FR and 25 days after beginning of RFD (day 125). Body fat and muscle weights were determined at day 131.ResultsIn spite of higher relative food intake (FI), BW was lower in L pigs. In L pigs, physical activity was lower at age 76 and 83 days compared to N pigs. IUGR did not affect EE or RMR, but resulted in higher COX and lower FOX, causing greater and earlier onset of fat deposition. During FR, EE and RMR of R pigs dropped below that of C pigs, and BW gain was delayed by 30 % irrespective of birth weight. In response to FR, COX decreased and FOX increased. During FR, in LR pigs FOX was ~50 % of that in NR pigs. After 4 days, but not 25 days of RFD, EB and fat synthesis were higher in pigs previously subjected to FR, indicating early catch-up fat. In R pigs, BW and the abdominal fat proportion were lower at 131 days.ConclusionsDifferences in food intake and substrate oxidation pattern, but not in EE and RMR, between L and N pigs were reflected in higher body fat proportions but lower body and muscle weights in L pigs. Refeeding following FR was initially associated with increased FI, a more positive EB and a more intense stimulation of fat synthesis which did not persist after 25 days of refeeding.Electronic supplementary materialThe online version of this article (doi:10.1007/s00394-013-0567-x) contains supplementary material, which is available to authorized users.