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PubMed1997

Energy expended by low birth weight infants in the deposition of protein and fat.

One hundred twenty low birth weight infants were enterally fed diets containing fixed differences in protein and energy content. Serial, biweekly measurements were made of metabolizable energy intake, energy expenditure, nitrogen balance, and distribution of states of sleep, from the time the infants were receiving full enteral intakes (180 mL/kg.d) until weight reached 2200 g. Using multiple regression analysis of energy expenditure against protein stored, and metabolizable energy, the energy expended in the deposition of protein was calculated to be 5.5 kcal/g +/- 1.1 kcal/g (SE) and the energy cost of fat deposited was 1.6 kcal/g +/- 0.3 kcal/g (SE). Estimated maintenance energy expenditure of the nongrowing low birth weight infant was 42.3 +/- 3.2 kcal/kg/d. Variations in distribution of sleep state, an assessment of the activity state of the infant, did not explain additional variability in energy expenditure, after adjusting for protein and energy storage.

Dietary Fats↗

PubMed1988

Relationships between body fatness, adipose tissue distribution and blood pressure in men and women.

The relationships between body fatness, fat distribution and blood pressure (BP) were studied in 234 women and 238 men, aged 18-50 years. In both sexes, subcutaneous (s.c.) fat (assessed by the measurement of s.c. skinfolds) and percent body fat (measured by underwater weighing) were correlated significantly with diastolic (0.27 less than or equal to r less than or equal to 0.37, p less than 0.0005) and systolic (0.17 less than or equal to r less than or equal to 0.29, p less than 0.01) BP. In either sex, the proportion of s.c. trunk fat as reflected by the ratio of trunk/extremity skinfolds showed significant associations with diastolic (men: r = 0.35, women: r = 0.20, p less than 0.01) and systolic BP (men: r = 0.15, women: r = 0.17, p less than 0.05). Control for the effects of covariables potentially affecting BP (energy intake, energy expenditure, maximal oxygen consumption, cigarette smoking, alcohol intake and age) revealed significant effects of age and alcohol intake on BP in men. In women, only age appeared to be associated with BP variation. Partial correlations after control for age and alcohol intake indicated a significant association between the trunk/extremity skinfolds ratio and diastolic BP in men. Such a correlation was not found in women after control for the effect of age. Analysis of variance (2 x 2 factorial with fixed effects) confirmed that, in men, the distribution of s.c. body fat was, per se, associated with diastolic BP (F = 8.43, p less than 0.01), whereas the proportional of s.c. trunk fat was not related to systolic BP in both sexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1989

Use of the doubly labeled water method for measurement of energy expenditure, total body water, water intake, and metabolizable energy intake in humans and small animals.

The basis of the doubly labeled water method is measurement of the differential rates of disappearance of two isotopes of water (H2 18O and either 2H2O or 3H2O, administered at the start of the study) from body water. Published studies indicate that, in its current forms, this technique can be used to provide accurate and reasonably precise information on carbon dioxide production, total body water, and water intake in free-living humans and many small animals. Total energy expenditure can be calculated from carbon dioxide production with little loss of precision. Metabolizable energy intake can also be predicted, as the sum of total energy expenditure plus an estimate for the change in body energy stores during the measurement, but this prediction is unlikely to be accurate and precise unless the subject is in approximate energy balance.

Animals↗

PubMed1988

Is obesity an eating disorder?

Obesity arises when energy intake exceeds energy expenditure over a long period. Excess weight has an energy value of 7000 kcal/kg. Theoretically excess weight might be gained either because energy expenditure was too low or energy intake was too high. Many studies have shown that on average obese people expand more energy than normal so, notwithstanding dietary histories to the contrary, they must on average have a higher energy intake to maintain body weight. However it is not possible to show that obese people have any significant defect in short-term regulation of energy intake. The likeliest hypothesis is that obesity is a disorder arising from a failure of the long-term regulation of energy intake, in which cognitive factors play an important part.

Cognition↗

PubMed2000

Dietary fat intake and regulation of energy balance: implications for obesity.

Obesity represents a major threat to health and quality of life. Although obesity has strong genetic determinants, the increasing prevalence of obesity in populations around the world suggests that environmental factors are promoting or exacerbating the problem. Experts are calling for public health efforts to deal with the global epidemic of obesity. Such a campaign would require that we identify and modify environmental factors that promote obesity. Our current food supply is high in fat, and high fat diets have been suggested to promote obesity by increasing energy intake, thus increasing the probability of positive energy balance and weight gain. However, others argue that high fat diets are not promoting obesity. In this paper, we review evidence from animal studies, carefully controlled laboratory studies, cross-sectional studies, clinical trials and studies in individuals at high risk to develop obesity. Although there are many environmental factors promoting excess energy intake and discouraging energy expenditure, it is clear that consumption of a high fat diet increases the likelihood of obesity and that the risk of obesity is low in individuals consuming low fat diets. On the basis of the available data, the current public health recommendations to lower dietary fat intake appear to be appropriate.

Animals↗

PubMed1999

[Home and outside home food complementarity in Bamako (Mali): nutritional and economic aspects. What is the rationality behind consumers' choices?].

BACKGROUND: Great modifications in social and family relationships and life style come from rapid urbanisation in developing countries. Various types of malnutrition coexist in these towns. Food consumption outside the home is more and more common. This in turn encourages rapid growth in the food informal economic sector which must be taken into account in food and nutrition policy and planning. The aim of this study was to analyse the characteristics and complementarities between home and outside the home food consumption of different kinds of individuals coming from different kinds of families in Bamako, in terms of expenditures and aspects of food and nutritional intakes. METHODS: 366 individuals from 74 families were interviewed. They were chosen according to defined criteria in three districts of Bamako of high, middle and poor socio-economic level. RESULTS: At home the daily food expenditure is 2.27 and 3.79 times greater per individual in rich than in middle income and poor families respectively. Animal proteins are respectively 41%, 19% and 9% of daily protein intake. Energy from lipids is 20 to 30% in rich and middle families. In poor ones it is only 15% which is the lower limit of nutritional recommendations. Moreover, contrary to proteins and carbohydrates, the cost of lipids seems, almost incompressible. Almost everybody eats out of home food, particularly children. Its cost, on an energy basis, is higher than home food. The expense is 19 to 27% of the family food budget. It appears necessary to the satisfaction of nutritional requirements in middle income and poor families. Despite various costs, whatever be the socio-economic level, energy intakes coming from that food are equivalent in absolute terms among various kinds of individuals: children, men and women. CONCLUSION: Families had to adapt their food strategies after the 1994 Franc CFA devaluation. Various hypotheses are presented, linked to intra-family relationships and, within poor families, to insertion in the street food economic sector, in order to understand, the logic of food choices. Such an analysis, where health, nutritional, economic, social and cultural aspects of food are taken into account, allows some concrete orientations for urban food and nutrition policy.

Adolescent↗

PubMed1992

Effects of feeding diets containing calcium salts of long-chain fatty acids to lactating dairy cows.

Four cows were utilized in a 4 x 4 Latin square design to investigate the effects of feeding Ca salts of long-chain fatty acids. Treatments were control diet with 1) no added fat, 2) 3% Ca salts of long-chain fatty acids, 3) 6% Ca salts of long-chain fatty acids, and 4) 9% Ca salts of long-chain fatty acids. Cows were fed chopped alfalfa hay, alfalfa haylage, corn silage, and concentrate (15:22:13:50) on a DM basis. Dry matter intake, energy intake, and ruminal fermentation were not altered greatly until Ca salts of long-chain fatty acids constituted 9% of DMI. Digestibilities of DM, OM, ADF, NDF, and hemicellulose were not affected by treatment. Digestibilities of cellulose, soluble residue, total C18 fatty acids, and total fatty acids followed quadratic patterns. Absorption of N was increased linearly when fat was fed, but digestibility of Ca was decreased linearly. Milk production, CP, and SNF were not altered greatly by inclusion of 3 or 6% Ca salts of long-chain fatty acids in the diet, but inclusion of 9% Ca salts of long-chain fatty acids decreased their production. Calcium salts of long-chain fatty acids increased milk fat percentage and production of fat and FCM when fed as 3 or 6% of the dietary DM but decreased yields of milk fat and FCM when fed as 9%. Calcium salts of fatty acids can be fed to provide up to 6% of the dietary DM without deleterious effects on ruminal fermentation and digestibilities of most nutrients.

Animal Feed↗

PubMed1997

Total energy expenditure in infants with bronchopulmonary dysplasia is associated with respiratory status.

UNLABELLED: Growth failure is a well-known problem in infants with bronchopulmonary dysplasia (BPD). We studied BPD infants' total daily energy expenditure (Ee), nutritional balance, and growth in relation to their past and current clinical status. Applying the doubly labelled water technique, Ee was measured in nine preterm infants with BPD receiving supplemental oxygen (postnatal age 61 +/- 13 days) and nine matched controls (36 +/- 21 days) during a 6-day period. Energy and protein balance, past and present respiratory status, and growth were assessed as well. The results show that Ee was higher in the BPD infants compared to controls (73 +/- 9 vs 63 +/- 8 kcal/kg/day, P < 0.05), but their faecal energy loss was lower (P < 0.01). Weight gain, energy intake, energy cost of growth, protein retention, and physical activity were not different. The respiratory frequency (RR) in the BPD infants was elevated in comparison with controls (P < 0.01). Within the BPD group, RR was positively correlated with energy expenditure (regression equation: Ee [kcal/kg/day] = 26.3 + 0.71*RR [min-1]; r2 = 0.82, P < 0.001), and was the single most significant determinant of Ee. CONCLUSION: Total energy expenditure in BPD infants is elevated and is strongly associated with their respiratory status. These findings could be of practical value for the nutritional management in infants with severe BPD.

Anthropometry↗

PubMed2005

Effect of pioglitazone on body composition and energy expenditure: a randomized controlled trial.

BACKGROUND: Several clinical studies have demonstrated that body weight increases after treatment with thiazolidinediones (TZDs). Prior studies have demonstrated an increase in insulin-stimulated lipid storage in adipose tissue. Some, but not all, studies demonstrate reductions in visceral adipose tissue. Changes in body weight are the result of changes in energy intake, energy expenditure, or both. OBJECTIVES: Based on these findings, the primary aim of this study was to evaluate the effect of TZDs on visceral, subcutaneous, and total body fat. Secondary aims were to determine the effects of pioglitazone on (a) energy expenditure, (b) hunger and satiety, (c) blood lipids, and (d) the role of insulinemia/sulfonylurea usage on weight gain in patients with type 2 diabetes. SUBJECTS AND METHODS: We performed a randomized, double-blind, placebo-controlled trial in 48 men and women with type 2 diabetes who had not previously received treatment with TZDs. Patients were treated for 24 weeks with 45 mg/d of pioglitazone or a matching placebo. Body composition was measured by dual-energy x-ray absorptiometry. Visceral and subcutaneous fat were measured by computed tomography. Resting metabolic rate and thermogenic response to a test meal were measured by indirect calorimetry before and after a standardized meal. Hunger and satiety were measured with visual analog scales before and after the same test meal. Blood was collected for the measurement of fasting glucose and insulin levels, hemoglobin A 1c levels, and lipid content. RESULTS: Pioglitazone treatment resulted in a decrease in hemoglobin A(1c) level by 0.96 +/- 1.1% vs 0.11 +/- 0.8% in the placebo group (P < .005). Body weight and fat increased steadily in the patients treated with pioglitazone during the 6 months of the study (+3.9 +/- 3.1 kg at 6 months in pioglitazone-treated patients vs -0.8 +/- 3.4 kg in the placebo-treated patients). Subcutaneous fat in the trunk, arms, and legs were all increased in the pioglitazone-treated group. Visceral fat did not change significantly in either group. Neither resting metabolic rate nor the thermogenic responses to a meal were altered by pioglitazone. Subjective measures of hunger (visual analog scale) did not change with pioglitazone treatment. Triglycerides fell in the pioglitazone-treated group (-58.5 +/- 124 mg/dL, P < .003). Neither the prior use of sulfonylureas nor the level of insulinemia before treatment was a predictor of weight or fat change. CONCLUSION: Pioglitazone increased subcutaneous body fat, but not visceral fat. There was no measurable effect on energy expenditure or hunger/satiety. In contrast to the placebo-treated patient with diabetes, weight gain occurs in the face of falling hemoglobin A(1c) and triglyceride levels.

Adult↗

PubMed2002

Genetic factors as predictors of weight gain in young adult Dutch men and women.

OBJECTIVE: To investigate the association between DNA polymorphisms in several candidate genes for obesity and weight gain. Polymorphisms in these genes may contribute to weight gain through effects on energy intake, energy expenditure or adipogenesis. DESIGN AND METHODS: From two large cohorts in The Netherlands (total 17,500 adult men and women), we compared 286 subjects aged 20-40 y who gained an average of 12.8 kg (range 5.5-47 kg) during a mean follow-up of 6.8 y with 296 subjects who remained relatively constant over the same period with respect to occurrence of several polymorphisms in candidate genes of obesity and some lifestyle factors. Subjects who were dieting, were high alcohol consumers, were pregnant, changed their smoking status recently, or those who suffered from serious illnesses were excluded. Polymorphisms were determined in the LEPR-gene (LEPR Lys109Arg, LEPR Gln223Arg, LEPR Lys656Asn), in the UCP1 gene (A-G mutation at position-3826 5' region), in the UCP2 gene (Ala55Val, 45 bp Ins/Del), in the PPARG2 gene (Pro12Ala) and in the ADRB2 gene (Gly16Arg and Gln27Glu). RESULTS: With the exception of the Gly16Arg polymorphism in the ADRB2 gene in men (P = 0.04) and women (P = 0.05), and the Lys109Arg polymorphism in the LEPR gene in women, no statistically significant differences in the genotype and allele frequencies were observed between weight gainers and non-weight gainers. Weight gainers differed in some aspects of dietary habits and physical activity patterns: weight gainers consumed relatively more savory snacks and were less active during leisure time compared with non-weight gainers. CONCLUSION: Only variations in the ADRB2 gene and LEPR gene, may contribute to susceptibility to weight gain. None of the other studied genetic markers were clearly associated with weight gain. Further research is necessary to establish the role of lifestyle factors, or interactions between genes or between genes and lifestyle factors on weight gain with age.

Adult↗

PubMed1998

Physical activity, energy expenditure and fitness: an evolutionary perspective.

The model for human physical activity patterns was established not in gymnasia, athletic fields, or exercise physiology laboratories, but by natural selection acting over eons of evolutionary experience. This paper examines how evolution has determined the potential for contemporary human performance, and advances the experience of recently-studied hunter-gatherers as the best available (although admittedly imperfect) indicator of the physical activity patterns for which our genetically determined biology was originally selected. From the emergence of the genus Homo, over 2 million years ago (MYA), until the agricultural revolution of roughly 10000 years ago our ancestors were hunter-gatherers, so the adaptive pressures inherent in that environmental niche have exerted defining influence on human genetic makeup. The portion of our genome that determines basic anatomy and physiology has remained relatively unchanged over the past 40 000 years. Thus, the complex interrelationship between energy intake, energy expenditure and specific physical activity requirements for current humans remains very similar to that originally selected for Stone Age men and women who lived by gathering and hunting. Research investigating optimal physical activity for human health and performance can be guided by understanding the evolution of physical activity patterns in our species.

Animals↗

PubMed1997

Single gene obesities in rodents: possible relevance to human obesity.

Obesity is a complex phenotype which "resolves" the influences of genes, development and environment. In any individual - and in the same individual at different times of life - the relative influence of these factors may vary. In this sense, obesity is a prototype of many of the diseases now confronting medical science. Among the most important concepts regarding such phenotypes is the idea that relevant genes mediate susceptibility to disease in a specific environmental context, not the inevitable occurrence of the phenotype regardless of the environment. Individuals with otherwise potent genetic predisposition to obesity will be lean in an environment of food deprivation/high demand for physical activity, and individuals not genetically predisposed to obesity may become so in an environment that includes tasty, calorically dense foods and/or few inducements to physical activity. Thus, in any effort to elucidate the genetic bases for susceptibility to obesity, the "environment" in which the obesity is occurring remains a critical factor regarding what sorts of genes will be identified. Because the genes that mediate susceptibility to obesity may affect energy intake, energy expenditure and/or the partitioning of calories between lean tissues and fat, the ability to define the gross metabolic basis for the obesity is very important in determining which genes are relevant to the phenotype. Because it is so difficult to experimentally define/control the environment of humans, and because the attainment of an obese state may actually rectify the metabolic differences predisposing to obesity, animal models of obesity have been looked at intensively for clues to the relevant genes in humans. Over the past 40 years, a series of autosomal dominant (Yellow) and recessive (obese, diabetes, tubby, fat, fatty) obesity mutations have been described in mice and rats. The molecular cloning of all of these genes has been accomplished within the past 4 years, providing an exciting array of new reagents for the molecular analysis of obesity. These genes encode molecules that appear to interact in physiologic systems that influence body fat stores. The genes and their apparent functions are summarized in the Table . The locations of these genes in the genomes of rodents and human are known, as are their genetic structure/sequence. Thus, their role(s) in human obesity can now be assessed directly.

Animals↗

PubMed2003

The human body may buffer small differences in meal size and timing during a 24-h wake period provided energy balance is maintained.

Because approximately 20% of the work force in the industrialized world have irregular working hours, it is pertinent to study the consequences of eating at irregular, especially nighttime hours. We studied the postprandial responses during nocturnal fasting vs. eating throughout a 24-h wake period. Seven healthy males were studied twice in a crossover design. After a 6-d diet adjustment period [high fat diet, 45 energy percent (en%) fat, 40 en% carbohydrates)] with sleep from 2300 to 0700 h, the men were kept awake for 24 h at the metabolic ward and given either 6 isoenergetic meals, i.e., every 4 h (N-eat) or 4 isoenergetic meals from 0800 to 2000 h followed by a nocturnal fast (N-fast), with the same 24-h energy intake. Energy expenditure, substrate utilization, activity, heat release, body temperature and blood variables were measured over 24 h. Energy expenditure and blood glucose, triacylglycerol, insulin and glucagon concentrations were lower and nonesterified fatty acids concentrations were higher during the nocturnal fast than during nocturnal eating (P < 0.05); however, no 24-h differences between the protocols were apparent. Nocturnal fasting slightly altered the secretory patterns of the thyroid hormones and cortisol (P < 0.05). We found no clear indication that it would be more favorable to ingest few larger daytime meals than smaller meals throughout the 24-h period. The body seems to be able to buffer small differences in meal size and timing provided energy balance is maintained.

Adaptation, Physiological↗

PubMed2005

Diabetes, obesity, and the brain.

Recent evidence suggests a key role for the brain in the control of both body fat content and glucose metabolism. Neuronal systems that regulate energy intake, energy expenditure, and endogenous glucose production sense and respond to input from hormonal and nutrient-related signals that convey information regarding both body energy stores and current energy availability. In response to this input, adaptive changes occur that promote energy homeostasis and the maintenance of blood glucose levels in the normal range. Defects in this control system are implicated in the link between obesity and type 2 diabetes.

Adipose Tissue↗

PubMed2002

Uncoupling proteins and thermoregulation.

Energy balance in animals is a metabolic state that exists when total body energy expenditure equals dietary energy intake. Energy expenditure, or thermogenesis, can be subcategorized into groups of obligatory and facultative metabolic processes. Brown adipose tissue (BAT), through the activity of uncoupling protein 1 (UCP1), is responsible for nonshivering thermogenesis, a major component of facultative thermogenesis in newborn humans and in small mammals. UCP1, found in the mitochondrial inner membrane in BAT, uncouples energy substrate oxidation from mitochondrial ATP production and hence results in the loss of potential energy as heat. Mice that do not express UCP1 (UCP1 knockouts) are markedly cold sensitive. The recent identification of four new homologs to UCP1 expressed in BAT, muscle, white adipose tissue, brain, and other tissues has been met by tremendous scientific interest. The hypothesis that the novel UCPs may regulate thermogenesis and/or fatty acid metabolism guides investigations worldwide. Despite several hundred publications on the new UCPs, there are a number of significant controversies, and only a limited understanding of their physiological and biochemical properties has emerged. The discovery of UCP orthologs in fish, birds, insects, and even plants suggests the widespread importance of their metabolic functions. Answers to fundamental questions regarding the metabolic functions of the new UCPs are thus pending and more research is needed to elucidate their physiological functions. In this review, we discuss recent findings from mammalian studies in an effort to identify potential patterns of function for the UCPs.

Adipose Tissue↗

PubMedDate not supplied

Fourth Daniel C. Baker, Jr. memorial lecture. Energy and the larynx.

Review of the logistics of energy supply in animals indicates that the advent of the larynx was part of a response to an earlier energy crisis. It permitted a major increase in the flow of energy available to the organism and became the mechanical control point and rate-limiting factor of the increased inflow. Phylogenetically, a succession of structural innovations steadily enhanced the flow capacity of the larynx and rendered the mechanism more versatile, most recently with the accrual of phonation (in mammals), pressurized closure (in primates and odontocetes), and vocal formants and efficiency (in man). The larynx is thus a marker of the animal's capabilities for energy intake, energy utilization and information emmission and, apparently, of the size and complexity of the brain. Today's energy crises appear to continue those of the past.

Anatomy, Comparative↗

PubMed2024

Prediction of metabolic syndrome using machine learning approaches based on genetic and nutritional factors: a 14-year prospective-based cohort study.

INTRODUCTION: Metabolic syndrome is a chronic disease associated with multiple comorbidities. Over the last few years, machine learning techniques have been used to predict metabolic syndrome. However, studies incorporating demographic, clinical, laboratory, dietary, and genetic factors to predict the incidence of metabolic syndrome in Koreans are limited. In the present study, we propose a genome-wide polygenic risk score for the prediction of metabolic syndrome, along with other factors, to improve the prediction accuracy of metabolic syndrome. METHODS: We developed 7 machine learning-based models and used Cox multivariable regression, deep neural network (DNN), support vector machine (SVM), stochastic gradient descent (SGD), random forest (RAF), Naïve Bayes (NBA) classifier, and AdaBoost (ADB) to predict the incidence of metabolic syndrome at year 14 using the dataset from the Korean Genome and Epidemiology Study (KoGES) Ansan and Ansung. RESULTS: Of the 5440 patients, 2,120 were considered to have new-onset metabolic syndrome. The AUC values of model, which included sex, age, alcohol intake, energy intake, marital status, education status, income status, smoking status, dried laver intake, and genome-wide polygenic risk score (gPRS) Z-score based on 344,447 SNPs (p-value < 1.0), were the highest for RAF (0.994 [95% CI 0.985, 1.000]) and ADB (0.994 [95% CI 0.986, 1.000]). CONCLUSIONS: Incorporating both gPRS and demographic, clinical, laboratory, and seaweed data led to enhanced metabolic syndrome risk prediction by capturing the distinct etiologies of metabolic syndrome development. The RAF- and ADB-based models predicted metabolic syndrome more accurately than the NBA-based model for the Korean population.

Humans↗

PubMed2006

Differential role of SH2-B and APS in regulating energy and glucose homeostasis.

SH2-B and APS, two members of a pleckstrin homology and SH2 domain-containing adaptor family, promote both insulin and leptin signaling in a similar fashion in cultured cells. In addition, APS mediates insulin-stimulated activation of the c-Cbl/CAP/TC10 pathway in cultured adipocytes. Here we characterized genetically modified mice lacking SH2-B, APS, or both to determine the physiological roles of these two proteins in animals. Disruption of the SH2-B gene resulted in obesity, hyperglycemia, hyperinsulinemia, and glucose intolerance. Conversely, deletion of the APS gene did not alter adiposity, energy balance, and glucose metabolism. Energy intake, energy expenditure, fat content, body weight, and plasma insulin, leptin, glucose, and lipid levels were similar between APS(-/-) and WT littermates fed either normal chow or a high-fat diet. Moreover, deletion of APS failed to alter insulin and glucose tolerance. APS(-/-)/SH2-B(-/-) double knockout mice also developed energy imbalance, obesity, hyperleptinemia, hyperinsulinemia, hyperglycemia, and glucose intolerance; however, plasma leptin and insulin levels were significantly lower in APS(-/-)/SH2-B(-/-) than in SH2-B(-/-) mice. These results suggest that SH2-B, but not APS, is a key positive regulator of energy and glucose metabolism in mice.

Adaptor Proteins, Signal Transducing↗