Overfeeding Diet Research Articles

Effects of overfeeding in breastfeeding period on blood pressure and vascular endothelial dilation function of rats

Objective To study the effects of postnatal overfeeding and high-fat diet on blood pressure of rats, and to explore the pathophysiological mechanism underlying hypertension induced by continuous early postnatal overfeeding. Methods Male Sprague-Dawley rats were randomly divided into normal feeding group (10/litter) and overfeeding group (3/litter) on postnatal day 3 with a random number table. After weaning at postnatal week 3, the rats were randomly given standard chow or high-fat (HF) diet until week 16. Hence four groups were analyzed, namely normal feeding group, breastfed overfeeding group, post-weaning overfeeding group, and continuous overfeeding group. Body weight was continuously monitored in each week. Visceral fat pad(retroperitoneal and perigenital), systolic pressure, and heart rate were observed at week 3 and week 16. Thoracic aorta was sampled for measurement of vascular endothelial dilation function. Histological morphology was observed with HE staining, nitric oxide content of thoracic aorta was detected with nitrate reductase method. The mRNA expression of endothelial nitric oxide synthase (eNOS) in thoracic aorta was determined by real-time polymerase chain reaction. The protein expressions of eNOS and phosphorylated eNOS were determined by Western blot. Results At week 3, breastfed overfeeding rats displayed significantly larger body weight [(77.80±0.57) g vs. (62.80±0.85)g, t=14.576, P<0.01] and visceral fat [retroperitoneal: (8.19±0.49)mg/g vs. (4.92±0.31)mg/g, t=5.629, P<0.01; perigenital: (3.50±0.29)mg/g vs. (2.08±0.13)mg/g, t=4.552, P<0.01] compared with normal feedindg rats, and the protein expression of phosphorylated eNOS in aortic tissues was significantly reduced to week 16 (F=15.215, P<0.01); high-fat diet feeding after weaning further increased the body weight and fat mass in breastfed overfeeding rats. At week 16, continuous overfeeding rats showed hypertension [(149±1.94)mmHg (1 mmHg=0.133 kPa), F=22.834, P<0.01], impaired vascular endothelial dilation function (F=7.648, P<0.05), and reduced protein expression of phosphorylated eNOS(F=15.215, P<0.01), while the post-weaning overfeeding group only had elevated blood pressure. Conclusions Overfeeding in breastfeeding period and high-fat diet after weaning leads to hypertension. The continuous decrease in phosphorylated eNOS in vascular tissues may be an important molecular process participating in the occurrence of vascular endothelial dysfunction in adults induced by postnatal overfeeding. Key words: Early postnatal overfeeding; Vascular endothelial dilation function; Hypertension; Nitric oxide; Phosphorylated endothelial nitric oxide synthase

Influence of amount and form of sorghum in the diet on the performance of overfed geese

SUMMARY Feeding has high economic and environmental costs in poultry production. The feeding of waterfowl for fatty liver production is largely based on the use of maize as an energy source. The aim of this trial was to study the effect of the form of presentation (whole grain or flour) and the amount (40.5, 56, or 100%, depending on the form) of sorghum in the overfeeding diet on the performance of geese. During overfeeding, a diet mainly composed of sorghum reduced the FCR of the geese and increased the weight of fatty liver, but reduced their commercial grading. The use of sorghum during geese overfeeding offers interesting prospects for a more sustainable fatty liver production system. Indeed, it could reduce the environmental effect of goose feeding while improving the flexibility of production systems, making it possible to use a cereal other than maize for overfeeding.

Extent and Determinants of Thermogenic Responses to 24 Hours of Fasting, Energy Balance, and Five Different Overfeeding Diets in Humans

Individual variation in the ability to convert excess calories to heat and the effects of dietary macronutrient composition are unclear. Stability and determinants of the energy expenditure (EE) response to overconsumption were assessed. Twenty subjects (75% male) with normal glucose regulation were evaluated during 24 hours each of energy balance, fasting, and 5 different diets with 200% energy requirements in a clinical research unit. Five 1-day overfeeding diets were given in random order: high carbohydrate (75%) and low protein (3%); high carbohydrate and normal protein (20%); high fat (46%) and low protein; high fat (60%) and normal protein; and balanced (50% carbohydrates, 20% protein). The 24-hour EE, sleeping EE, and thermic effect of food (TEF) during each diet were measured with a metabolic chamber. Appetitive hormones were measured before and after the diets. The EE response to overfeeding exhibited good intraindividual reproducibility. Similar increases above eucaloric feeding in 24-hour EE (mean 10.7 ± 5.7%, P < .001; range 2.9-18.8%) and sleeping EE (14.4 ± 11.3%, P < .001; range 1.0-45.1%) occurred when overfeeding diets containing 20% protein, despite differences in fat and carbohydrate content, but the EE response during overfeeding diets containing 3% protein was attenuated. The percent body fat negatively correlated with TEF during normal protein overfeeding (r = -0.53, P < .01). Fasting peptide YY negatively correlated with TEF (r = -0.56, P < .01) and the increase in sleeping EE (r = -0.54, P < .01) during overfeeding. There is an intrinsic EE response to overfeeding that negatively associates with adiposity, although it represents a small percentage of consumed calories.

Effects of short-term high-fat overfeeding on genome-wide DNA methylation in the skeletal muscle of healthy young men

Energy-dense diets that are high in fat are associated with a risk of metabolic diseases. The underlying molecular mechanisms could involve epigenetics, as recent data show altered DNA methylation of putative type 2 diabetes candidate genes in response to high-fat diets. We examined the effect of a short-term high-fat overfeeding (HFO) diet on genome-wide DNA methylation patterns in human skeletal muscle. Skeletal muscle biopsies were obtained from 21 healthy young men after ingestion of a short-term HFO diet and a control diet, in a randomised crossover setting. DNA methylation was measured in 27,578 CpG sites/14,475 genes using Illumina's Infinium Bead Array. Candidate gene expression was determined by quantitative real-time PCR. HFO introduced widespread DNA methylation changes affecting 6,508 genes (45%), with a maximum methylation change of 13.0 percentage points. The HFO-induced methylation changes were only partly and non-significantly reversed after 6-8weeks. Alterations in DNA methylation levels primarily affected genes involved in inflammation, the reproductive system and cancer. Few gene expression changes were observed and these had poor correlation to DNA methylation. The genome-wide DNA methylation changes induced by the short-term HFO diet could have implications for our understanding of transient epigenetic regulation in humans and its contribution to the development of metabolic diseases. The slow reversibility suggests a methylation build-up with HFO, which over time may influence gene expression levels.

Measurement of Ad Libitum Food Intake, Physical Activity, and Sedentary Time in Response to Overfeeding

Given the wide availability of highly palatable foods, overeating is common. Energy intake and metabolic responses to overfeeding may provide insights into weight gain prevention. We hypothesized a down-regulation in subsequent food intake and sedentary time, and up-regulation in non-exercise activity and core temperature in response to overfeeding in order to maintain body weight constant. In a monitored inpatient clinical research unit using a cross over study design, we investigated ad libitum energy intake (EI, using automated vending machines), core body temperature, and physical activity (using accelerometry) following a short term (3-day) weight maintaining (WM) vs overfeeding (OF) diet in healthy volunteers (n = 21, BMI, mean ± SD, 33.2±8.6 kg/m2, 73.6% male). During the ad libitum periods following the WM vs. OF diets, there was no significant difference in mean 3-d EI (4061±1084 vs. 3926±1284 kcal/day, p = 0.41), and there were also no differences either in core body temperature (37.0±0.2°C vs. 37.1±0.2°C, p = 0.75) or sedentary time (70.9±12.9 vs. 72.0±7.4%, p = 0.88). However, during OF (but not WM), sedentary time was positively associated with weight gain (r = 0.49, p = 0.05, adjusted for age, sex, and initial weight). In conclusion, short term overfeeding did not result in a decrease in subsequent ad libitum food intake or overall change in sedentary time although in secondary analysis sedentary time was associated with weight gain during OF. Beyond possible changes in sedentary time, there is minimal attempt to restore energy balance during or following short term overfeeding.Trial RegistrationClinicalTrials.gov NCT00342732

Impact of short-term high-fat feeding and insulin-stimulated FGF21 levels in subjects with low birth weight and controls

Fibroblast growth factor 21 (FGF21) is a metabolic factor involved in glucose and lipid metabolism. However, little is known about the physiological role of FGF21 during a dietary challenge in humans. Twenty healthy low birth weight (LBW) with known risk of type 2 diabetes and 26 control (normal birth weight (NBW)) young men were subjected to 5 days of high-fat (HF) overfeeding (+50%). Basal and clamp insulin-stimulated serum FGF21 levels were examined before and after the diet, and FGF21 mRNA expression was measured in muscle and fat biopsies respectively. Five days of HF overfeeding diet significantly (P<0.001) increased fasting serum FGF21 levels in both the groups (P<0.001). Furthermore, insulin infusion additionally increased serum FGF21 levels to a similar extent in both the groups. Basal mRNA expression of FGF21 in muscle was near the detection limit and not present in fat in both the groups before and after the dietary challenge. However, insulin significantly (P<0.001) increased FGF21 mRNA in both muscle and fat in both the groups during both diets. Short-term HF overfeeding markedly increased serum FGF21 levels in healthy young men with and without LBW but failed to increase muscle or fat FGF21 mRNA levels. This suggests that the liver may be responsible for the rise of serum FGF21 levels during overfeeding. In contrast, the increase in serum FGF21 levels during insulin infusion may arise from increased transcription in muscle and fat. We speculate that increased serum FGF21 levels during HF overfeeding may be a compensatory response to increase fatty acid oxidation and energy expenditure.

Expression and nutritional regulation of the (pro)renin receptor in rat visceral adipose tissue.

Early life nutritional environment plays an important role in the development of visceral adipose tissue and interacts with nutritional regulations in adulthood, leading to metabolic dysregulations. We hypothesized that the renin-angiotensin system may play a role in the programming-induced development of visceral adipose tissue. We studied, using a model of programming of overweight and glucose intolerance, obtained by post-natal overfeeding with consecutive highfat diet, the status of plasma renin activity and mesenteric adipose renin-angiotensin system, including the recently identified (pro)renin receptor, in adult rats. Post-natal overfeeding or high-fat feeding lead to overweight with increased visceral fat mass and adipocytes surface. When both paradigms were associated, adipocytes surface showed a disproportionate increase. A strong immunoreactivity for (pro)renin receptor was found in stromal cells. Plasma renin activity increased in programmed animals whereas (pro)renin receptor expressing cells density was stimulated by high-fat diet. There was a positive, linear relationship between plasma renin activity and (pro)renin receptor expressing cells density and adipocytes surface. Our experiments demonstrate that association of post-natal overfeeding and high-fat diet increased plasma renin activity and adipose (pro)renin receptor expression. Such phenomenon could explain, at least in part, the associated disproportionate adipocyte hypertrophy and its accompanying increased glucose intolerance.

Fasting during exercise for fitness during feasting?

Fasting during exercise for fitness during feasting?

Whole-body calorimetry studies in adult men. 2. The interaction of exercise and over-feeding on the thermic effect of a meal.

Studies have claimed that an enhancement of the thermic effect of a meal (TEM) is an important adaptive mechanism to account for energy wastage during over-feeding. Eight healthy normal-weight young men were studied during 1 week on a weight-maintenance diet and again during 1 week when they were over-fed by 50% with fat. During each experimental week, the subject occupied a whole-body indirect calorimeter at 26 degrees for two separate periods of 36 h. The periods differed in the amount of exercise they contained. The thermic responses to the identical meals were measured during rest on one occasion and during exercise on a bicycle ergometer on the other. On the maintenance diet the absolute TEM (kJ/min) was 1.51 (SD 0.42) at rest and 1.31 (SD 0.75) during exercise (no significant difference). The equivalent values (kJ/min) on the over-feeding diet were 2.2 (SD 0.48) and 1.97 (SD 0.64) (no significant difference). The absence of a significant interaction between TEM and exercise was also demonstrated by the fact that the effect of over-feeding on total 24 h energy expenditure was unaffected by the subject's level of physical activity while in the calorimeter. In conclusion, the present study has provided no evidence to support the hypothesis that TEM is enhanced during exercise.

Whole-body calorimetry studies in adult men. 1. The effect of fat over-feeding on 24 h energy expenditure.

Eight young men of normal weight were maintained for 1 week on a weight-maintenance diet followed by a 1-week period of over-feeding with extra fat designed to increase energy intake by 50%. Two 36 h calorimetry sessions with low and high physical activities were included in each feeding period. Faecal and urine collections permitted checks on energy malabsorption and nitrogen excretion. Over-feeding led to increases in body-weight, faecal energy and N excretion and in estimated N retention. Faecal energy outputs on the maintenance and over-feeding diets were 5 and 4.4% of the respective gross energy intakes. Energy expenditure on fat over-feeding increased by 5.6% on the low-activity regimen and 6.4% on the high-activity regimen. This amounted, in terms of the extra energy intake, to 9 and 11% on the inactive and active schedules respectively. The increase affected day- and night-time rates of energy expenditure plus the basal metabolic rate. Individuals with a low percentage body fat showed the greatest response to over-feeding. Nutrient-balance studies derived from calorimetry suggested that fat over-feeding led to substantial fat deposition with no evidence of sparing of carbohydrate oxidation. The theoretical cost of depositing dietary fat was exceeded, suggesting that regulatory thermogenic mechanisms may have been stimulated to a small extent.