Energy expenditure in humans: effects of dietary fat and carbohydrate

1990 ◽  
Vol 258 (2) ◽  
pp. E347-E351 ◽  
Author(s):  
W. G. Abbott ◽  
B. V. Howard ◽  
G. Ruotolo ◽  
E. Ravussin
Keyword(s):  
Energy Expenditure ◽  
Dietary Fat ◽  
Weight Maintenance ◽  
Caloric Intake ◽  
Insulin Dependent Diabetes Mellitus ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Pima Indians ◽  
High Fat ◽  
High Carbohydrate

A high-dietary fat intake may be an important environmental factor leading to obesity in some people. The mechanism could be either a decrease in energy expenditure and/or an increase in caloric intake. To determine the relative importance of these mechanisms we measured 24-h energy expenditure in a whole body calorimeter in 14 nondiabetic subjects and in six subjects with non-insulin-dependent diabetes mellitus, eating isocaloric, weight-maintenance, high-fat, and high-carbohydrate diets. All subjects were Pima Indians. In nondiabetics, the mean total 24-h energy expenditure was similar (2,436 +/- 103 vs. 2,359 +/- 82 kcal/day) on high-fat and high-carbohydrate diets, respectively. The means for sleeping and resting metabolic rates, thermic effect of food, and spontaneous physical activity were unchanged. Similar results were obtained in the diabetic subjects. In summary, using a whole body calorimeter, we found no evidence of a decrease in 24-h energy expenditure on a high-fat diet compared with a high-carbohydrate diet.

scholarly journals Food intake and energy expenditure are increased in high-fat-sensitive but not in high-carbohydrate-sensitive obesity-prone rats

2014 ◽  
Vol 307 (3) ◽  
pp. R299-R309 ◽  
Author(s):  
Dalila Azzout-Marniche ◽  
Catherine Chaumontet ◽  
Nachiket A. Nadkarni ◽  
Julien Piedcoq ◽  
Gilles Fromentin ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Caloric Intake ◽  
Specific Pattern ◽  
High Fat ◽  
High Carbohydrate ◽  
Burst Intensity ◽  
Activity Burst ◽  
Parallel Increase ◽  
Male Wistar Rats ◽  
Reduced Activity

Obesity-prone (OP) rodents are used as models of human obesity predisposition. The goal of the present study was to identify preexisting defects in energy expenditure components in OP rats. Two studies were performed. In the first one, male Wistar rats ( n = 48) were fed a high-carbohydrate diet (HCD) for 3 wk and then a high-fat diet (HFD) for the next 3 wk. This study showed that adiposity gain under HCD was 2.9-fold larger in carbohydrate-sensitive (CS) than in carbohydrate-resistant (CR) rats, confirming the concept of “carbohydrate-sensitive” rats. Energy expenditure (EE), respiratory quotient (RQ), caloric intake (CI), and locomotor activity measured during HFD identified no differences in EE and RQ between fat-resistant (FR) and fat-sensitive (FS) rats, and indicated that obesity developed in FS rats only as the result of a larger CI not fully compensated by a parallel increase in EE. A specific pattern of spontaneous activity, characterized by reduced activity burst intensity, was identified in FS rats but not in CS ones. This mirrors a previous observation that under HCD, CS but not FS rats, exhibited bursts of activity of reduced intensity. In a second study, rats were fed a HFD for 3 wk, and the components of energy expenditure were examined by indirect calorimetry in 10 FR and 10 FS rats. This study confirmed that a low basal EE, reduced thermic effect of feeding, defective postprandial energy partitioning, or a defective substrate utilization by the working muscle are not involved in the FS phenotype.

Hypertension in CB57BL/6J mouse model of non-insulin-dependent diabetes mellitus

1993 ◽  
Vol 264 (1) ◽  
pp. R73-R78 ◽  
Author(s):  
E. Mills ◽  
C. M. Kuhn ◽  
M. N. Feinglos ◽  
R. Surwit
Keyword(s):  
Diabetes Mellitus ◽  
Heart Rate Response ◽  
Control Diet ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
High Fat ◽  
Insulin Dependent ◽  
Hypotensive Response ◽  
Simple Carbohydrate

The C57BL/6J (BL/6) mouse develops non-insulin-dependent diabetes mellitus (NIDDM) when fed a high fat-high simple carbohydrate (HFHSC) diet, whereas A/J mice do not. The purpose of the study was to determine whether hypertension occurred with NIDDM and whether it was sustained by sympathetic nervous system (SNS) hyperactivity. After 3 mo on an HFHSC diet with a low Na content (0.06%), awake, tail-cuff systolic blood pressure (BP) increased 20% above the control diet in BL/6 (138 +/- 3 vs. 115 +/- 4) but not in A/J (115 +/- 6 vs. 113 +/- 2 mmHg) mice. On a normal Na (0.4%)-HFHSC diet, BL/6 mice had a higher BP than on 0.06% Na (149 +/- 3 at 3 mo, 162 +/- 6 at 4.5 mo). After 1 mo on the 0.06% Na-HFHSC diet, direct BP of anesthetized BL/6 mice was 18% higher than control. The hypotensive response to interruption of SNS activity by ganglionic blockade (chlorisondamine) increased in the BL/6 mice (50%), whereas the heart rate response increased in both strains (20-30%). Analysis of variance (ANOVA) on glucose detected significant effects of strain and diet and a strain x diet interaction (P = 0.0007). At 1 or 3 mo, HFHSC-fed BL/6 mice were hyperglycemic (> 11 mM) compared with diet or strain controls. The ANOVA on insulin detected strain and diet effects but not a strain x diet interaction (P = 0.3). HFHSC increased insulin above the control of 140-160 pM in A/J and BL/6 strain (20-70% at 1 mo, 400% at 3 mo).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Dietary Fat and Sugar Differentially Affect β-Adrenergic Stimulation of Cardiac ERK and AKT Pathways in C57BL/6 Male Mice Subjected to High-Calorie Feeding

2020 ◽  
Vol 150 (5) ◽  
pp. 1041-1050
Author(s):  
Sadia Ashraf ◽  
Gizem Yilmaz ◽  
Xu Chen ◽  
Romain Harmancey
Keyword(s):  
Signaling Pathways ◽  
Dietary Fat ◽  
Tolerance Test ◽  
Whole Body ◽  
Adrenergic Stimulation ◽  
High Fat ◽  
Cardiac Growth ◽  
Regulatory Pathways ◽  
High Sugar ◽  
Stimulation Of

ABSTRACT Background High dietary fat and sugar promote cardiac hypertrophy independently from an increase in blood pressure. The respective contribution that each macronutrient exerts on cardiac growth signaling pathways remains unclear. Objective The goal of this study was to investigate the mechanisms by which high amounts of dietary fat and sugar affect cardiac growth regulatory pathways. Methods Male C57BL/6 mice (9 wk old; n = 20/group) were fed a standard rodent diet (STD; kcal% protein-fat-carbohydrate, 29-17-54), a high-fat diet (HFD; 20-60-20), a high-fat and high-sugar Western diet (WD; 20-45-35), a high-sugar diet with mixed carbohydrates (HCD; 20-10-70), or a high-sucrose diet (HSD; 20-10-70). Body composition was assessed weekly by EchoMRI. Whole-body glucose utilization was assessed with an intraperitoneal glucose tolerance test. After 6 wk on diets, mice were treated with saline or 20 mg/kg isoproterenol (ISO), and the activity of cardiac growth regulatory pathways was analyzed by immunoblotting. Data were analyzed by ANOVA with data from the STD group included for references only. Results Compared with HCD and HSD, WD and HFD increased body fat mass 2.7- to 3.8-fold (P < 0.001), induced glucose intolerance (P < 0.001), and increased insulin concentrations >1.5-fold (P < 0.05), thereby enhancing basal and ISO-stimulated AKT phosphorylation at both threonine 308 and serine 473 residues (+25−63%; P < 0.05). Compared with HFD, the high-sugar diets potentiated ISO-mediated stimulation of the glucose-sensitive kinases PYK2 (>47%; P < 0.05 for HCD and HSD) and ERK (>34%; P < 0.05 for WD, HCD, and HSD), thereby leading to increased phosphorylation of protein synthesis regulator S6K1 at threonine 389 residue (>64%; P < 0.05 for WD, HCD, and HSD). Conclusions Dietary fat and sugar affect cardiac growth signaling pathways in C57BL/6 mice through distinct and additive mechanisms. The findings may provide new insights into the role of overnutrition in pathological cardiac remodeling.

scholarly journals Reproducibility of 24 h energy expenditure measurements using a human whole body indirect calorimeter

1987 ◽  
Vol 57 (2) ◽  
pp. 201-209 ◽  
Author(s):  
Janna O. De Boer ◽  
Aren J. H. Van Es ◽  
Joop E. Vogt ◽  
Joop M. A. Van Raaij ◽  
Joseph G. A. J. Hautvast
Keyword(s):  
Energy Expenditure ◽  
Coefficient Of Variation ◽  
Weight Maintenance ◽  
Metabolizable Energy ◽  
Whole Body ◽  
Time Interval ◽  
Daily Routine ◽  
Individual Level ◽  
Period 2 ◽  
Significant Difference

1. Ten female subjects completed two similar experimental procedures (periods 1 and 2) to obtain values of reproducibility of energy intake and 24 h energy expenditure (24hEE) measurements in a whole body indirect calorimeter. The periods consisted of consumption of a provided weight-maintenance diet for 6–8 d, faeces and urine collection during the last 4 d and occupation of the calorimeter during the last 3 d. The daily routine inside the calorimeter simulated a sedentary day in normal life with some physical activity: 8 h sleep, 75 min bicycling and the remaining time spent on sedentary activities. The metabolizable energy (ME) content of the diet (14% energy as protein, 46% energy as carbohydrate, 40% energy as fat) was calculated using food tables. The actual ME intake as well as digestibility and metabolizability of the diet were obtained later by analyses of food, faeces and urine for energy. Three consecutive 24hEE measurements were performed during the stay in the calorimeter in each period. The time interval between the two periods varied from 2 to 24 months. Reproducibility was assessed at group and individual level.2. Mean digestibility and metabolizability of the diet showed no significant difference between periods. The within-subject coefficient of variation of metabolizability between periods was 1.7%.3. Mean 24hEE (MJ) over 3 d did not differ between period 1 (8.78 (SD 0.63)) and period 2 (8.73 (SD 0.66)). The within-subject coefficient of variation in mean 24hEE over three successive days between periods was 3.1% but decreased, after deletion of values for subjects who were less adapted to the calorimeter, to 1.9%.4. The results are discussed with regard to length of trial and the number of subjects required to test a difference in energy metabolism using whole body indirect calorimeters.

scholarly journals APP deficiency results in resistance to obesity but impairs glucose tolerance upon high fat feeding

2018 ◽  
Vol 237 (3) ◽  
pp. 311-322 ◽  
Author(s):  
Juliane K Czeczor ◽  
Amanda J Genders ◽  
Kathryn Aston-Mourney ◽  
Timothy Connor ◽  
Liam G Hall ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Cell Mass ◽  
Tolerance Test ◽  
Whole Body ◽  
Dark Phase ◽  
High Fat ◽  
Neuronal Metabolism ◽  
Fat Feeding ◽  
Deficient Mice

The amyloid precursor protein (APP) generates a number of peptides when processed through different cleavage mechanisms, including the amyloid beta peptide that is implicated in the development of Alzheimer’s disease. It is well established that APP via its cleaved peptides regulates aspects of neuronal metabolism. Emerging evidence suggests that amyloidogenic processing of APP can lead to altered systemic metabolism, similar to that observed in metabolic disease states. In the present study, we investigated the effect of APP deficiency on obesity-induced alterations in systemic metabolism. Compared with WT littermates, APP-deficient mice were resistant to diet-induced obesity, which was linked to higher energy expenditure and lipid oxidation throughout the dark phase and was associated with increased spontaneous physical activity. Consistent with this lean phenotype, APP-deficient mice fed a high-fat diet (HFD) had normal insulin tolerance. However, despite normal insulin action, these mice were glucose intolerant, similar to WT mice fed a HFD. This was associated with reduced plasma insulin in the early phase of the glucose tolerance test. Analysis of the pancreas showed that APP was required to maintain normal islet and β-cell mass under high fat feeding conditions. These studies show that, in addition to regulating aspects of neuronal metabolism, APP is an important regulator of whole body energy expenditure and glucose homeostasis under high fat feeding conditions.

Glucose turnover in presence of changing glucose concentrations: error analysis for glucose disappearance

1995 ◽  
Vol 269 (3) ◽  
pp. E557-E567 ◽  
Author(s):  
A. Caumo ◽  
M. Homan ◽  
H. Katz ◽  
C. Cobelli ◽  
R. Rizza
Keyword(s):  
Error Analysis ◽  
Glucose Uptake ◽  
Specific Activity ◽  
Insulin Dependent Diabetes Mellitus ◽  
Postprandial Glucose ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Glucose Turnover ◽  
Glucose Disappearance ◽  
Analytic Expressions

The present studies were undertaken to determine whether 1) the cold- and hot-GINF techniques used with Steele's model provide equivalent estimates of the rates of glucose appearance (R(a)) and disappearance (R(d)) in the presence of physiological changes in glucose and insulin concentrations, 2) the conditions for the best estimation of R(a) are the same as those for R(d), 3) the magnitude of error (if present) differs in diabetic and nondiabetic subjects, and 4) situations exist in which the knowledge of R(d) allows inferences to be made on whole body glucose uptake. To do so we performed experiments in non-insulin-dependent diabetes mellitus and nondiabetic subjects using simultaneous infusions of [6-3H]glucose and [6-14C]glucose; glucose and insulin were infused to mimic normal postprandial glucose and insulin profiles; the infused glucose contained [6-14C]glucose but not [6-3H]glucose. Compared with the hot-GINF method, the traditional cold-GINF method underestimated (P < 0.05) R(a) and R(d) by 10-15% and hepatic glucose release by 25-50% during the 1st h of the study, with the magnitude of error being the same in both diabetic and nondiabetic subjects. Error analysis demonstrated that errors in R(a) and R(d) have different analytic expressions containing common structural but different volume errors. Both R(a) and R(d) can be accurately measured in diabetic and nondiabetic subjects if glucose specific activity is kept constant and the volume of the accessible pool is used to calculate glucose disappearance. The relationship between R(d) and whole body glucose uptake was also derived. Although R(d) can be determined by relying on measurements in the accessible pool only, the assessment of whole body glucose uptake requires a model of the nonaccessible portion of the glucose system. However, knowledge of R(d) can provide useful insights into the behavior of whole body glucose uptake.

Effects of dietary protein restriction on regional amino acid metabolism in insulin-dependent diabetes mellitus

1996 ◽  
Vol 270 (1) ◽  
pp. E148-E157 ◽  
Author(s):  
I. G. Brodsky ◽  
J. T. Devlin
Keyword(s):  
Diabetes Mellitus ◽  
Dietary Protein ◽  
Protein Intake ◽  
Insulin Dependent Diabetes Mellitus ◽  
Protein Restriction ◽  
Insulin Dependent Diabetes ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Dietary Protein Restriction ◽  
Insulin Dependent

We studied subjects with insulin-dependent diabetes mellitus (IDDM) and controls by administering primed continuous infusions of L-[1-13C,15N)]leucine and L-[2,3-13C2]alanine to measure whole body and forearm metabolism of these amino acids during ample protein intake and again after 4 wk of moderately restricted protein intake. Decreased rates of whole body protein degradation, leucine transamination, leucine oxidation, and increased forearm alanine release produced by dietary protein restriction occurred equivalently in IDDM subjects under short-term tightly managed glycemia and in controls. Dietary protein restriction did not affect whole body alanine appearance or forearm leucine appearance, disposal, or balance in IDDM subjects or controls. IDDM subjects differed from controls only in that normal forearm leucine balance was maintained at higher rates of leucine appearance and disposal. We conclude that IDDM subjects adapt normally to dietary protein restriction. Undernutrition during moderate protein deprivation in these patients likely occurs during episodes of poor glycemic control.

Effect of diet on triolein absorption in weanling rats

1990 ◽  
Vol 258 (1) ◽  
pp. G38-G44 ◽  
Author(s):  
C. A. Flores ◽  
P. M. Brannon ◽  
M. A. Wells ◽  
M. Morrill ◽  
O. Koldovsky
Keyword(s):  
Dietary Fat ◽  
Intact Animal ◽  
Fat Intake ◽  
Fat Absorption ◽  
High Fat ◽  
High Carbohydrate ◽  
Weanling Rats ◽  
Low Carbohydrate ◽  
Triton Wr 1339

To determine the effect of altered dietary fat intake on the rate of fat absorption in the intact animal, we fed male weanling rats either a high fat-low carbohydrate (HF-LC) (calories: 67% fat, 10% carbohydrate, 20% protein) or low fat-high carbohydrate (LF-HC) (calories: 10% fat, 67% carbohydrate, 20% protein) diet for 8 days. Absorption of [14C]triolein was estimated by determining 1) 14CO2 expiration in breath, 2) intestinal triglyceride output using Triton WR-1339, an inhibitor of lipoprotein lipase, and 3) quantitating the disappearance of labeled triolein from the gastrointestinal tract. Changes in the activity of pancreatic lipase and amylase confirmed the adaptation to altered fat and carbohydrate intake. Animals fed the HF-LC diet exhibited approximately twofold greater triolein disappearance, oxidation, and intestinal triglyceride output compared with animals fed LF-HC. There was also a highly significant linear relationship between 14CO2 excretion and intestinal triglyceride output in both diet groups. These data show that high dietary fat content markedly enhances in vivo fat absorption in the weanling rat.

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