Body Weight Balance Research Articles

Effects of prepartum controlled-energy wheat straw and grass hay diets supplemented with starch or sugar on periparturient dairy cow performance and lipid metabolism

This study examined the effects of a forage source [wheat straw (WS) versus grass hay (GH)] prepartum and supplemental carbohydrate source [corn (dry feed; DF) versus molasses (liquid feed; LF)] on pre- and postpartum intake, digestibility, selective particle consumption, milk yield, and lipid metabolism. The objectives were to determine if forage or pre- and postpartum supplement alters periparturient intake, energy balance, and milk yield. Sixty (n=15) multiparous dairy cows were used in a randomized complete block design with a 2×2 factorial arrangement of treatments to compare WS versus GH diets supplemented with either DF or LF. Dietary treatments were (1) WS prepartum + DF pre- and postpartum (WSDF), 2) WS prepartum + LF pre- and postpartum (WSLF), (3) GH prepartum + DF pre- and postpartum (GHDF), and (4) GH prepartum + LF pre- and postpartum (GHLF). Treatments began at dry-off, × before expected calving. During the prepartum phase, cows maintained dry matter intake (DMI) at 2.0% of body weight and prepartum energy balance remained positive for all treatments until calving. Prepartum GH diets had a more positive energy balance compared with WS diets. On week −5, energy balance was more positive for GHDF than for WSDF or GHLF. Energy balance for WSLF, however, was lower on week −3 and −1 than GHDF. Liquid feed decreased dry matter digestibility and increased prepartum liver triglyceride, serum nonesterified fatty acids (NEFA), and tended to increase β-hydroxybutyrate. After calving, LF decreased DMI and energy balance, but not yield of milk or 3.5% fat-corrected milk, resulting in greater feed efficiency compared with DF. Forage did not affect postpartum DMI, but milk yield tended to be higher for WS versus GH. The DMI expressed as percentage of body weight was not affected by supplement or prepartum forage type. Cows fed WS had lower serum NEFA, higher liver glycogen, and tended to have a lower triglyceride to glycogen ratio postpartum than GH. Serum NEFA peaked on d 14 for all treatments and then declined thereafter. In postpartum diets, more particles were retained on the top screen for LF (>19.0mm) of the Penn State Particle Separator, which also tended to have more particles in the second screen (particles 19.0–8.0mm). Supplement had minimal effect on postpartum selective particle consumption. In conclusion, feeding diets containing WS resulted in lower postpartum serum NEFA, higher liver glycogen, and a tendency for greater milk production and lower liver triglyceride to glycogen than those containing GH. Liquid feed reduced postpartum DMI but not yield of milk yield or 3.5% fat-corrected milk yield, resulting in an improvement in feed efficiency. Future research should continue to investigate the use of single dry cow diet feeding strategies as they affect pre- and postpartum animal responses.

Shp2 Controls Female Body Weight and Energy Balance by Integrating Leptin and Estrogen Signals

In mammals, leptin regulates food intake and energy balance mainly through the activation of LepRb in the hypothalamus, and estrogen has a leptin-like effect in the hypothalamic control of metabolism. However, it remains to be elucidated how estrogen signaling is intertwined with the leptin pathway. We show here that Shp2, a nonreceptor tyrosine phosphatase, acts to integrate leptin and estrogen signals. The expression of a dominant-active mutant (Shp2(D61A)) in forebrain neurons conferred female, but not male, transgenic mice resistance to high-fat diet (HFD)-induced obesity and liver steatosis, accompanied by improved insulin sensitivity and glucose homeostasis. Fed with either HFD or regular chow food, Shp2(D61A) female mice showed dramatically enhanced leptin sensitivity. Microinjection of Shp2(D61A)-expressing adeno-associated virus into mediobasal hypothalamus elicited a similar antiobese effect in female mice. Biochemical analyses showed a physical association of Shp2 with estrogen receptor alpha, which is necessary for the synergistic and persistent activation of Erk by leptin and estrogen. Together, these results elucidate a mechanism for the direct cross talk of leptin and estrogen signaling and offer one explanation for the propensity of postmenopausal women to develop obesity.

Promoter methylation of serotonin transporter gene is associated with obesity measures: a monozygotic twin study

Objective:Epigenetic mechanisms are increasingly being recognized as an important factor for obesity. The serotonin transporter gene (SLC6A4) has a critical role in regulating food intake, body weight and energy balance. This study examines the potential association between SLC6A4 promoter methylation and obesity measures in a monozygotic (MZ) twin sample.Methods:We studied 84 MZ twin pairs drawn from the Vietnam Era Twin Registry. Obesity measures include body mass index (BMI), body weight, waist circumference (WC) and waist-hip ratio (WHR). The SLC6A4 promoter methylation profile in peripheral blood leukocytes was quantified by bisulfite pyrosequencing. The association between methylation variation and obesity parameters was examined by mixed-model regression and matched pair analysis, adjusting for age, smoking, alcohol consumption, physical activity and total daily energy intake. Multiple testing was controlled using the adjusted false discovery rate (q-value).Results:Mean methylation level was positively correlated with BMI (r=0.29; P=0.0002), body weight (r=0.31; P<0.0001) and WC (r=0.20; P=0.009), but not WHR. Intra-pair differences in mean methylation were significantly correlated with intra-pair differences in BMI, body weight and WC, but not WHR. On average, a 1% increase in mean methylation was associated with 0.33 kg m−2 increase in BMI (95% CI: 0.02–0.65; P=0.03), 1.16 kg increase in body weight (95% CI, 0.16–2.16; P=0.02) and 0.78 cm increase in WC (95% CI, 0.05–1.50; P=0.03) after controlling for potential confounders.Conclusions:SLC6A4 promoter hypermethylation is significantly associated with an increased prevalence of obesity within a MZ twin study.

Diet and Obesity

Obesity can be defined as a state of excess body fat or body energy stores in excess of physiological needs. The prevalence of obesity has increased dramatically throughout the world. Despite the greater understanding of the physiologic mechanisms regulating body weight and energy balance, the causes of human obesity poorly understood. Much of human obesity is multifactorial and usually involves relative over-consumption of food. And, consumption of high-fat diets is implicated in the etiology of obesity. Fat-derived energy intake has increased in Korea. Changes in gastric motor and sensory functions can be associated with development of obesity. A High-fat diet may facilitate adaptive changes that contribute to the development of obesity through reduced postprandial satiation in persons with a high baseline maximum tolerated volume. A high fat intake may influences the central control of appetite and behavioral choices in food intake. Further well-controlled large studies with a longer preload duration in Koreans to elucidate the presence and extent of gastrointestinal sensory, motor, absorptive, and behavioral adaptations to diets enriched with specific macronutrients. (Korean J Med 2012;82:291-297)

Analysis of the show jumping competition according to the type of seat and the way of driving into the obstacle. Part II Analiza konkursów skoków przez przeszkody w zależności od rodzaju dosiadu i sposobu najazdu. Część II

A perfect synchronization of the rider and the horse is an art requiring a lot of skill and intuition as well as advanced horse training. The correct body-weight balance allows the rider to smoothly change the riding positions. While observing the riders on the jumping courses we can note a wide variety of riding positions in the distance ride as well as approaching the obstacle. The research was conducted during competitions in show jumping. The analysis was based on 80 riders participating in 4 competitions, 27 of which were not of Polish nationality. The total of 93 horses was taken into consideration. Special attention was paid to the sitting position in different elements of the round (arches, turns, lines etc.). There were three dominating riding positions: half seat – HS – 1, light seat – LS – 2, full seat – FS – 3. In order to show more detailed characteristics of the aforementioned riding positions three last fouls before the jump are presented in a so-called “sequence”. The most effective sequence in approaching verticals and double bars was sequence II (full seat – full seat – light seat), in case of oxers the least fault-prone was sequence I (3 full seats). The analysis showed that the best riders chose a light seat most frequently. However, it was the full seat that was chosen most often and the correlation between this riding position and the number of faults is significant.

Reduced Food Intake and Body Weight in Mice Deficient for the G Protein-Coupled Receptor GPR82

G protein-coupled receptors (GPCR) are involved in the regulation of numerous physiological functions. Therefore, GPCR variants may have conferred important selective advantages during periods of human evolution. Indeed, several genomic loci with signatures of recent selection in humans contain GPCR genes among them the X-chromosomally located gene for GPR82. This gene encodes a so-called orphan GPCR with unknown function. To address the functional relevance of GPR82 gene-deficient mice were characterized. GPR82-deficient mice were viable, reproduced normally, and showed no gross anatomical abnormalities. However, GPR82-deficient mice have a reduced body weight and body fat content associated with a lower food intake. Moreover, GPR82-deficient mice showed decreased serum triacylglyceride levels, increased insulin sensitivity and glucose tolerance, most pronounced under Western diet. Because there were no differences in respiratory and metabolic rates between wild-type and GPR82-deficient mice our data suggest that GPR82 function influences food intake and, therefore, energy and body weight balance. GPR82 may represent a thrifty gene most probably representing an advantage during human expansion into new environments.

Defective Hypothalamic Autophagy Directs the Central Pathogenesis of Obesity via the IκB Kinase β (IKKβ)/NF-κB Pathway

Autophagy has been recently demonstrated to control cell and tissue homeostasis, including the functions of various metabolic tissues. However, it remains unclear whether autophagy is critical for the central nervous system and particularly the hypothalamus for exerting metabolic regulation. Using autophagy-related protein 7 (Atg7) as an autophagic marker, this work showed that autophagy was highly active in the mediobasal hypothalamus of normal mice. In contrast, chronic development of dietary obesity was associated with autophagic decline in the mediobasal hypothalamus. To investigate the potential role of autophagy in the hypothalamic control of metabolic physiology, a mouse model was developed with autophagic inhibition in the mediobasal hypothalamus using site-specific delivery of lentiviral shRNA against Atg7. This model revealed that hypothalamic inhibition of autophagy increased energy intake and reduced energy expenditure. These metabolic changes were sufficient to increase body weight gain under normal chow feeding and exacerbate the progression of obesity and whole-body insulin resistance under high-fat diet feeding. To explore the underlying mechanism, this study found that defective hypothalamic autophagy led to hypothalamic inflammation, including the activation of proinflammatory IκB kinase β pathway. Using brain-specific IκB kinase β knockout mice, it was found that the effects of defective hypothalamic autophagy in promoting obesity were reversed by IκB kinase β inhibition in the brain. In conclusion, hypothalamic autophagy is crucial for the central control of feeding, energy, and body weight balance. Conversely, decline of hypothalamic autophagy under conditions of chronic caloric excess promotes hypothalamic inflammation and thus impairs hypothalamic control of energy balance, leading to accelerated development of obesity and comorbidities.

Hypoxia-Inducible Factor Directs POMC Gene to Mediate Hypothalamic Glucose Sensing and Energy Balance Regulation

Hypoxia-inducible factor (HIF) is a nuclear transcription factor that responds to environmental and pathological hypoxia to induce metabolic adaptation, vascular growth, and cell survival. Here we found that HIF subunits and HIF2α in particular were normally expressed in the mediobasal hypothalamus of mice. Hypothalamic HIF was up-regulated by glucose to mediate the feeding control of hypothalamic glucose sensing. Two underlying molecular pathways were identified, including suppression of PHDs by glucose metabolites to prevent HIF2α degradation and the recruitment of AMPK and mTOR/S6K to regulate HIF2α protein synthesis. HIF activation was found to directly control the transcription of POMC gene. Genetic approach was then employed to develop conditional knockout mice with HIF inhibition in POMC neurons, revealing that HIF loss-of-function in POMC neurons impaired hypothalamic glucose sensing and caused energy imbalance to promote obesity development. The metabolic effects of HIF in hypothalamic POMC neurons were independent of leptin signaling or pituitary ACTH pathway. Hypothalamic gene delivery of HIF counteracted overeating and obesity under conditions of nutritional excess. In conclusion, HIF controls hypothalamic POMC gene to direct the central nutrient sensing in regulation of energy and body weight balance.

Neuropeptide Exocytosis Involving Synaptotagmin-4 and Oxytocin in Hypothalamic Programming of Body Weight and Energy Balance

Hypothalamic neuropeptides play essential roles in regulating energy and body weight balance. Energy imbalance and obesity have been linked to hypothalamic signaling defects in regulating neuropeptide genes; however, it is unknown whether dysregulation of neuropeptide exocytosis could be critically involved. This study discovered that synaptotagmin-4, an atypical modulator of synaptic exocytosis, is expressed most abundantly in oxytocin neurons of the hypothalamus. Synaptotagmin-4 negatively regulates oxytocin exocytosis, and dietary obesity is associated with increased vesicle binding of synaptotagmin-4 and thus enhanced negative regulation of oxytocin release. Overexpressing synaptotagmin-4 in hypothalamic oxytocin neurons and centrally antagonizing oxytocin in mice are similarly obesogenic. Synaptotagmin-4 inhibition prevents against dietary obesity by normalizing oxytocin release and energy balance under chronic nutritional excess. In conclusion, the negative regulation of synaptotagmin-4 on oxytocin release represents a hypothalamic basis of neuropeptide exocytosis in controlling obesity and related diseases.

Maternal exposure to multi‐wall carbon nanotubes does not induce embryo–fetal developmental toxicity in rats

Although the potential risk of carbon nanotubes (CNTs) to humans has recently increased due to expanding production and widespread use, the potential adverse effects of CNTs on embryo-fetal development have not yet been determined. This study investigated the potential effects of multi-wall CNTs (MWCNTs) on pregnant dams and embryo-fetal development in rats. MWCNTs were administered to pregnant rats by gavage at 0, 40, 200, and 1,000 mg/kg/day. All dams were subjected to Cesarean section on day 20 of gestation, and the fetuses were examined for any morphological abnormalities. All animals survived to the end of the study. A decrease in thymus weight was observed in the high dose group in a dose-dependent manner. However, maternal body weight, food consumption, and oxidant-antioxidant balance in the liver were not affected by treatment with MWCNTs. No treatment-related differences in gestation index, fetal deaths, fetal and placental weights, or sex ratio were observed between the groups. Morphological examinations of the fetuses demonstrated no significant difference in incidences of abnormalities between the groups. The results show that repeated oral doses of MWCNTs during pregnancy induces minimal maternal toxicity and no embryo-fetal toxicity at 1,000 mg/kg/day in rats. The no-observed-adverse-effect level of MWCNTs is considered to be 200 mg/kg/day for dams and 1,000 mg/kg/day for embryo-fetal development. In this study, the dosing formulation was not analyzed to determine the degree of reaggregation (or not), nor were blood levels of CNT's measured in the dosed animals to verify or characterize absorption.

Deficiency of Lipoprotein Lipase in Neurons Modifies the Regulation of Energy Balance and Leads to Obesity

Free fatty acids (FFAs) suppress appetite when injected into the hypothalamus. To examine whether lipoprotein lipase (LPL), a serine hydrolase that releases FFAs from circulating triglyceride (TG)-rich lipoproteins, might contribute to FFA-mediated signaling in the brain, we created neuron-specific LPL-deficient mice. Homozygous mutant (NEXLPL-/-) mice were hyperphagic and became obese by 16weeks of age. These traits were accompanied by elevations in the hypothalamic orexigenic neuropeptides, AgRP and NPY, and were followed by reductions in metabolic rate. The uptake of TG-rich lipoprotein fatty acids was reduced in the hypothalamus of 3-month-old NEXLPL-/- mice. Moreover, deficiencies in essential fatty acids in the hypothalamus were evident by 3months, with major deficiencies of long-chain n-3 fatty acids by 12months. These results indicate that TG-rich lipoproteins are sensed in the brain by an LPL-dependent mechanism and provide lipid signals for the central regulation of body weight and energy balance.

The Genetic Polymorphisms in Leptin Gene Locus (Obesity Gene) in Romanian Farm Species and Their Evaluation as Genetic Markers in Breeding and Traceability

Leptin is a key hormone which modulates the neuroendocrine control fat reserves in organism, appetite, body weight and energy balance (Leifers et al. 2002). The leptin gene (obesity gene) polymorphism was associated in different farm species with different quantitative and qualitative characters with an increased economic importance (Carsai et al. 2005). In cattle the A allele was associated with a high quality meat and carcasses, a higher milk quantity and quality (Leifers et al. 2002). Identification of some polymorphisms in leptin gene and establishment of some associations between these genotypes and food consumption, daily weight gain, adipose tissue quantity, carcass weight, milk quantity and quality, represents a solution for optimization and speeding up of breeding process, by early use in selection of the information provided by this genetic marker.

Identification and genetic effects of a novel polymorphism in the distal promoter region of porcine leptin gene

Leptin is a hormone expressed mainly in white adipose tissue. It acts on satiety centers in the hypothalamus, and by binding to particular receptor OB-Rb, plays a crucial role in controlling appetite, body weight, fat amount and total energy balance. In this study, a novel single nucleotide polymorphism (SNP), i.e., SNP G-2863A, was identified in the distal promoter region of porcine leptin gene. Totally 780 individuals of Duroc, Yorkshire, Laiwu, Lulai Black breeds, and Landrace × Yorkshire crossbred were genotyped by PCR-SSCP approach. The effects of SNP G-2863A on mRNA and serum protein levels of leptin as well as in driving transcription were examined. The results showed that, except for Duroc and Yorkshire pigs, three genotypes of GG, GA and AA were detected. Allele G occurred with a higher frequency in western breeds and Landrace × Yorkshire crossbred pigs, whereas with a lower frequency in Laiwu pigs. Statistical analysis indicated that there were consistent trends toward higher levels in animals with genotype GG than with GA or AA genotypes in backfat thickness of both Landrace × Yorkshire crossbred and Lulai Black pigs, in backfat leptin mRNA and the circulating serum leptin protein level in half-sibling Lulai Black pigs, and the activity of allele G was significantly higher than allele A (P < 0.01) in driving reporter gene expression. These results suggest that SNP G-2863A is a potential DNA marker for backfat thickness and has a regulatory role in leptin transcription.

Task-specificity vs. ceiling effect: Step-training in shallow water after spinal cord injury

While activity-based rehabilitation is one of the most promising therapeutic approaches for spinal cord injury, the necessary components for optimal locomotor retraining have not yet been determined. Currently, a number of different activity-based approaches are being investigated including body weight-supported treadmill training (with and without manual assistance), robotically-assisted treadmill training, bicycling and swimming, among others. We recently showed, in the adult rat, that intensive rehabilitation based on swimming brought about significant improvements in hindlimb performance during swimming but did not alter the normal course of recovery of over-ground walking ( Smith et al., 2006a,b, 2009). However, swimming lacks the phasic limb-loading and plantar cutaneous feedback thought to be important for weight-supported step training. So, we are investigating an innovative approach based on walking in shallow water where buoyancy provides some body weight support and balance while still allowing for limb-loading and appropriate cutaneous afferent feedback during retraining. Thus, the aim of this study is to determine if spinal cord injured animals show improved overground locomotion following intensive body weight-supported locomotor training in shallow water. The results show that training in shallow water successfully improved stepping in shallow water, but was not able to bring about significant improvements in overground locomotion despite the fact that the shallow water provides sufficient body weight support to allow acutely injured rats to generate frequent plantar stepping. These observations support previous suggestions that incompletely injured animals retrain themselves while moving about in their cages and that daily training regimes are not able to improve upon this already substantial functional improvement due to a ceiling effect, rather than task-specificity, per se. These results also support the concept that moderately-severe thoracic contusion injuries decrease the capacity for body weight support, but do not decrease the capacity for pattern generation. In contrast, animals with severe contusion injuries could not support their body weight nor could they generate a locomotor pattern when provided with body weight support via buoyancy.

Physical activity, food intake, and body weight regulation: insights from doubly labeled water studies

Body weight and energy balance can be maintained by adapting energy intake to changes in energy expenditure and vice versa, whereas short-term changes in energy expenditure are mainly caused by physical activity. This review investigates whether physical activity is affected by over- and undereating, whether intake is affected by an increase or a decrease in physical activity, and whether being overweight affects physical activity. The available evidence is based largely on studies that quantified physical activity with doubly labeled water. Overeating does not affect physical activity, while undereating decreases habitual or voluntary physical activity. Thus, it is easier to gain weight than to lose weight. An exercise-induced increase in energy requirement is typically compensated by increased energy intake, while a change to a more sedentary routine does not induce an equivalent reduction of intake and generally results in weight gain. Overweight and obese subjects tend to have similar activity energy expenditures to lean people despite being more sedentary. There are two ways in which the general population trend towards increasing body weight can be reversed: reduce intake or increase physical activity. The results of the present literature review indicate that eating less is the most effective method for preventing weight gain, despite the potential for a negative effect on physical activity when a negative energy balance is reached.

Effect of 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors (statins) on adipose tissue

Statins are competitive inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, a rate-limiting enzyme in cholesterol synthesis. Statins are widely used in the treatment of hypercholesterolemia and to reduce risk of acute cardiovascular and cerebrovascular events. Statins inhibit synthesis of not only cholesterol but also of non-steroid isoprenoids such as farnesyl- and geranylgeranylpyrophosphate, coenzyme Q (ubiquinone), dolichol, etc., which are involved in multiple cell metabolic and signaling cascades. Adipose tissue may be an important target for statins. Although statins have no effect on body weight and energy balance, they inhibit differentiation of preadipocytes to mature adipocytes and may induce adipocyte apoptosis. Stimulation of lipoprotein lipase in adipose tissue accelerates VLDL metabolism and may contribute to triglyceride-lowering effect of statins. According to some studies, statins reduce insulin sensitivity of adipose tissue and impair glucose metabolism in adipocytes. Statins also inhibit adipose tissue inflammation which plays an important role in obesity-associated pathologies. Finally, statins modulate production of adipokines such as leptin, adiponectin, resistin and visfatin. Currently available data suggest that effects on adipose tissue contribute to both beneficial and adverse consequences of statin therapy. Adipobiology 2009; 1: 35-50.

Central NMU signaling in body weight and energy balance regulation: evidence from NMUR2 deletion and chronic central NMU treatment in mice

To investigate the role of the central neuromedin U (NMU) signaling system in body weight and energy balance regulation, we examined the effects of long-term intracerebroventricular (icv) infusion of NMU in C57Bl/6 mice and in mice lacking the gene encoding NMU receptor 2. In diet-induced obese male and female C57BL/6 mice, icv infusion of NMU (8 microg x day(-1) x mouse(-1)) for 7 days decreased body weight and total energy intake compared with vehicle treatment. However, these parameters were unaffected by NMU treatment in lean male and female C57BL/6 mice fed a standard diet. In addition, female (but not male) NMUR2-null mice had increased body weight and body fat mass when fed a high-fat diet but lacked a clear body weight phenotype when fed a standard diet compared with wild-type littermates. Furthermore, female (but not male) NMUR2-null mice fed a high-fat diet were protected from central NMU-induced body weight loss compared with littermate wild-type mice. Thus, we provide the first evidence that long-term central NMU treatment reduces body weight, food intake, and adiposity and that central NMUR2 signaling is required for these effects in female but not male mice.

Early Life Origins of Obesity: Role of Hypothalamic Programming

The incidence of obesity is increasing at an alarming rate and this worldwide epidemic represents an ominous predictor of increases in diseases such as type 2 diabetes and metabolic syndrome. Epidemiological and animals studies suggest that maternal obesity and alterations in postnatal nutrition are associated with increased risks for obesity, hypertension, and type 2 diabetes in the offspring. Furthermore, there is also growing appreciation that developmental programming of neuroendocrine systems by the perinatal environment represents a possible cause for these diseases. This review article provides a synthesis of recent evidence concerning the actions of perinatal hormones and nutrition in programming the development and organization of hypothalamic circuits that regulate body weight and energy balance. Particular attention is given to the neurodevelopmental actions of insulin and leptin.

Acclimation to Heat During Incubation: 3. Body Weight, Cloacal Temperatures, and Blood Acid-Base Balance in Broilers Exposed to Daily High Temperatures

The aim of the present study was to investigate the effects of parental age and heat acclimation during incubation on BW, cloacal temperature, and blood acid-base balance in fast-growing broilers exposed to daily cyclic high ambient temperatures from 21 to 42 d posthatch. Eggs obtained from 32- (younger), 42- (middle-aged), and 65-wk-old (older) breeders were divided into 2 groups. One group of eggs was incubated at the control incubation temperature (IT(CONT)) and the second group was heat acclimated at 38.5 degrees C for 6 h/d from d 10 to 18 of incubation (IT(HA)). Chicks were reared at standard brooding temperatures from d 1 to 21. From d 21 to 42, half of the broilers per incubation temperature and parental age were kept as controls (AT(CONT)) and the other half were exposed to daily cyclic heat treatment (AT(HIGH)) to impose a stress response. The reduction in BW at AT(HIGH) was more pronounced for progeny from older compared with younger parents. However, this reduction in BW was more or less abolished for broilers from eggs incubated at IT(HIGH), implying an increased tolerance to heat stress. Compared with IT(CONT,) IT(HA) reduced BW of broilers from 32- and 42-wk-old parents while having no effect on those from 65-wk-old parents when reared at AT(CONT). Higher blood pH, and lower partial pressure CO(2) and HCO(3)(-) at AT(HIGH) were associated with greater cloacal temperatures throughout the heat stress from d 21 to 42. Increases in cloacal temperature by AT(HIGH) were greater for IT(CONT) than for IT(HA) broilers. The AT(HIGH) and IT(HA) broilers had lesser blood partial pressure CO(2) concentrations than AT(CONT) and IT(CONT), respectively. Although at AT(HIGH), blood HCO(3)(-) was lower for broilers from all parental ages, it was more pronounced for those from 65-wk-old parents. It is concluded that these changes in blood acid-base balance reflected adaptive responses to heat stress, and incubating eggs at IT(HA) improved thermotolerance of fast-growing broilers.

Obesity makes for a big headline

Obesity makes for a big headline