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PubMed1988

A comparative study of smoking, drinking and dietary habits in population samples in France, Italy, Spain and Switzerland. I. Study design and dietary habits.

Diet, tobacco and alcohol consumption, and occupational histories have been investigated in stratified random samples of the adult population in 6 areas in France (departement of Calvados), Italy (province of Varese and city of Torino), Spain (provinces of Navarra and Zaragoza) and Switzerland (canton of Geneva), to be used as a reference group in a case-control study on cancer of the larynx and hypopharynx. Out of a total of 8,074 sampled subjects, 5,564 could be interviewed. Sampling procedures are described, and reasons for non-response are analysed. Everywhere the intake of the 4 energy providing nutrients (particularly alcohol) was much greater in men than in women. In both sexes, total caloric intake was higher in Calvados and in Italy than elsewhere. There were wide inter-area variations in the consumption of butter + milk products and oils, resulting in a polyunsaturated/saturated fatty acid ratio ranging from 0.27 in Calvados to 0.54-0.65 in Spain. Among nutrients suggested to be involved in cancer aetiology, inter-area differences in daily intake were up to 3-fold for carotene and smaller for vitamin C and fibre. The proportion of lipids, fibres, vitamin C and carotene provided by different foods varied widely between areas, thus suggesting that in etiological cancer studies consideration should be given not only to nutrients but also to foods providing them.

Adult↗
PubMed1999

Caloric restriction abolishes enhanced metabolic efficiency induced by ectopic agouti protein in yellow mice.

Caloric restriction (CR), from approximately 3 months of age, at 70% of the ad libitum (AL) caloric intake prevented development of overt obesity in female "viable yellow" Avy/A (BALB/cStCrlfC3Hf/Nctr x VY/WffC3Hf/Nctr-Avy) F1 hybrid mice. In adult yellow Avy/A mice, caloric restriction eliminated the increased metabolic efficiency associated with the presence of agouti protein in ectopic sites. At 4 weeks of age, the yellow Avy/A mice were approximately 14% heavier and by 12 weeks of age, when caloric restriction began, they were approximately 24% heavier than the congenic agouti A/a mice. Between 4 and 12 weeks, the yellow mice gained approximately 63% in body weight, whereas the agouti mice gained only approximately 44%. While the comparable AL Avy/A mice gained approximately 128% and the AL A/a mice gained approximately 41% between 12 and 51 weeks of age, the CR Avy/A and A/a mice gained only 16% and 15%, respectively. Mean brain weights of CR mice of both genotypes were lower than those of the comparable ad libitum-fed (AL) groups; however, CR Avy/A mice had slightly, but significantly (P < 0.0001), higher brain weights than CR A/a mice. The larger mean brain weight and retention, during caloric restriction, of the somewhat greater prerestriction Avy/A mean body weight compared with prerestriction A/a mice were consonant with the hypothesis that ectopic agouti protein affects somatic growth directly or indirectly. This may be related to altered developmental/metabolic programming in yellow mice, indicated by greater metabolic efficiency and by an early transient increase in circulating IGF-1 levels. The specific cellular processes modulated by the agouti protein in ectopic sites remain to be identified.

Age Factors↗
PubMed1998

Hyperglycemia in extremely- low-birth-weight infants.

The cause of hyperglycemia in extremely-low-birth-weight (ELBW) infants is not well understood. We studied infants weighing <1,000 g to investigate the relationship of hyperglycemia to blood levels of insulin-like growth factor (IGF)-I and IGF-II. We also compared two methods of treatment for hyperglycemia: continuous insulin infusion and reduction of glucose intake. Fifty-six ELBW infants were enrolled on day 2 of life. Intravenous glucose intake was increased incrementally to a maximum of 12 mg/kg/min on day 6. Infants who developed hyperglycemia were randomly assigned to receive reduced glucose intake (n = 11) or insulin infusion (n = 12). Infants whose blood sugar remained normal served as controls (n = 33). Blood was drawn on days 3, 8 and 15 in all infants, and again when they developed hyperglycemia. Nutritional intake and laboratory results for the treatment groups were compared with controls. Hyperglycemic infants had lower birth weights than controls. Hyperglycemic infants treated with glucose reduction remained <60 kcal/kg/day longer than control or insulin infusion groups (8.6 +/- 1.3 days vs. 4.1 +/- 0.2 and 5.5 +/- 0.6 days). No infants became hypoglycemic during insulin infusion. There was no difference in baseline blood levels of IGF-I or IGF-II among the groups, and these growth factors did not change in response to hyperglycemia. Hyperglycemic infants had baseline levels of insulin which were similar to normal controls, and endogenous insulin increased in response to hyperglycemia in 15 of the 23 infants who developed hyperglycemia. IGF-I and IGF-II are not related to hyperglycemia. In our population, hyperglycemic infants did not have baseline insulin deficiency and most had a normal insulin response to hyperglycemia. Insulin infusion appears safe in these infants and helped to maintain normal caloric intake, whereas glucose reduction was associated with a prolonged caloric deprivation.

Birth Weight↗
PubMed1994

Interrelationship between dietary lipids and calories and experimental mammary gland tumorigenesis.

The purpose of this communication was to review and critique the studies designed to examine the interrelationship between dietary fat and calories in experimental rodent mammary gland tumorigenesis. The results of these studies clearly show that hyperalimentation of fat, either saturated or unsaturated, significantly stimulates this tumorigenic process. This has been demonstrated in an impressive array of carcinogen-induced, transplantable, spontaneous, and metastatic experimental rodent mammary gland tumor systems. The stimulatory effect of high levels of dietary fat appears to act primarily at the promotional stage of this tumorigenic process. Whether the mammary tumor stimulatory effect of high levels of dietary fat is a result of the metabolic activity of the fat per se or is due to an excessive energy (caloric) intake has been examined. Data obtained from the experimental studies that address this issue support the viewpoint that the mammary tumorigenic-enhancing activities of a high fat diet is, at least in part, through a caloric mechanism.

Animals↗
PubMed2002

A double-blind, randomised, placebo controlled study on the influence of carbohydrate solution intake during labour.

OBJECTIVE: Although there has been much debate on whether women should be allowed to eat and drink during labour, little scientific data are available on the effects of caloric intake on the course of labour. DESIGN: Double-blind, randomised, placebo controlled. SETTING: Leyenburg Hospital, The Hague, The Netherlands. POPULATION: Two hundred and one consecutive nulliparous women, pregnant of a single fetus in cephalic presentation. METHODS: All women were included in early labour (2cm-4cm of cervical dilatation) and were allowed to drink at will. MAIN OUTCOME MEASURES: The duration of labour, the need for augmentation and pain medication and the incidence of abdominal and vaginal instrumental deliveries. RESULTS: Drinking of carbohydrate solutions was well tolerated, but did not show any beneficial effects regarding labour outcome when compared with the control group. In the carbohydrate group, a higher caesarean section rate was observed (RR 2.9, 95% CI 1.29-6.54). CONCLUSIONS: Women in the carbohydrate group had worse labour outcome. It is unclear whether a statistical coincidence, a negative effect of the carbohydrate intake or an incorrect carbohydrate intake strategy is responsible for these results. Further studies are necessary before any definite conclusion can be drawn.

Adult↗
PubMed2005

Enhancement of amphetamine-induced locomotor response in rats on different regimens of diet restriction and 2-deoxy-D-glucose treatment.

Diet restriction (DR) in rodents increases lifespan, reduces age-related disease and pathology, increases stress responses, and maintains better function later into life compared with conventional ad libitum (AL) feeding. We have been investigating different DR regimens and also DR mimetics that stimulate stress response pathways that are activated by DR. By inhibiting glycolysis, feeding or injection of 2-deoxy-D-glucose (2DG) has been proposed as a DR mimetic and has been shown to provide neuroprotection. In the current study, we examined whether 2DG treatment produces behavioral changes similar to those observed in DR rats following stimulation of the dopaminergic (DA) system by D-amphetamine (AMPH). Male Fischer 344 rats were maintained on different dietary regimens: 40% daily DR (40% DR); every-other-day feeding (EOD); or AL with some groups provided food containing 0.4% 2DG or injected i.p. with 2DG. In addition, we examined the persistence of effects of DR or 2DG feeding after switching rats to AL. When locomotor activity was assessed at different time points following initiation of dietary treatments, we noted that the enhancement of AMPH-induced locomotor responses emerged earlier in DR rats than observed in 2DG fed rats, but 40% DR and EOD rats responded in a similar manner. Enhanced locomotor responses persisted in 2DG fed rats even when returned to normal diet for 1 month and in the case of DR rats even after 2 months of AL feeding. Three weeks of 2DG injections also enhanced AMPH response, but this effect was transient. The most important finding was that 2DG did not affect body weight or diet intake yet had effects similar to DR. Thus, 2DG appears to activate DA pathways in the same direction as DR does but without the necessity of reducing caloric intake.

Amphetamine↗
PubMed1994

Tomatoes and risk of digestive-tract cancers.

In view of the persisting uncertainty concerning possible mechanisms by which high vegetable and fruit intake decreases cancer risk, foods with divergent values for potentially important micronutrients are a priority for investigation. Tomatoes are low in beta-carotene, but high in lycopene, an active antioxidative agent. In order to assess the effect of tomatoes on risk of cancers of the digestive tract, data were analyzed from an integrated series of case-control studies conducted between 1985 and 1991 in northern Italy, where tomato intake is high but, also, heterogeneous. The overall dataset included the following histologically confirmed cancer cases: oral cavity and pharynx, 314; esophagus, 85; stomach, 723; colon, 955; and rectum, 629; and a total of 2,879 controls admitted to hospital for acute non-neoplastic or non-digestive conditions, unrelated to long-term dietary modifications. Multivariate odds ratios (OR) and 95% confidence interval (CI) for subsequent quartiles of intake of raw tomatoes were derived, after allowance for age, sex, study center, education, smoking and drinking level, and tertile of total caloric intake. There was a consistent pattern of protection for all sites (OR in the upper quartile ranging between 0.4 and 0.7), most notably for gastrointestinal neoplasms. All trends in risk were highly significant. The beneficial effect of raw tomatoes in this population may be partly due to the fact that they constitute perhaps the most specific feature of the Mediterranean diet. However, if it is true that tomatoes protect against digestive-tract cancers, this is of interest from both a scientific and a public health viewpoint.

Aged↗
PubMedDate not supplied

Desmethionine-bombesin receptor antagonist blocks bombesin-induced inhibition of alcohol intake.

[D-Phe6,Des-Met14]bombesin(6-14), ethyl amide (D-BN) is a specific, competitive receptor antagonist of bombesin, a neuropeptide that inhibits alcohol and food intake. We tested the effects of IP injected D-BN (4-400 micrograms/kg) on bombesin-induced (4 micrograms/kg) reduction of caloric intake. In the first experiment, ad lib-fed female and male rats (Ns = 18) were deprived of water for 23 h, injected with peptides or saline in randomized sequences of doses, and immediately given access to 5% w/v ethanol for 30 min, followed by 30 min of water. In a second experiment, male rats (N = 10) were injected with the antagonist at 10 or 20 min prior to bombesin injection and alcohol access, and behaviors were observed and quantified once a minute with an instantaneous time-sampling technique. D-BN injection blocked the bombesin-induced reduction in alcohol intake (> or = 40 micrograms/kg) and food intake (> or = 200 micrograms/kg). When injected 20 min prior to access, D-BN alone (200 micrograms/kg) initially elevated alcohol drinking and later increased feeding behaviors and decreased resting, relative to saline injection. Results indicate bombesin-induced reduction of alcohol intake depends on a specific peptidergic receptor process, and endogenous bombesin-like peptide could act physiologically to elicit satiation with ethanol and food.

Alcohol Drinking↗
PubMed2004

Aggressive early total parental nutrition in low-birth-weight infants.

OBJECTIVE: This study aimed to compare nitrogen balance and biochemical tolerance of early aggressive versus late total parenteral nutrition in very-low-birth-weight (VLBW) infants over the first week of life. STUDY DESIGN: In all, 32 ventilator-dependent preterm infants were prospectively randomized into two groups. The Early Total Parenteral Nutrition (ETPN) group received 3.5 g/kilo-day amino acids (AA), and 3 g/kilo-day of 20% Intralipid (IL), starting within 1 hour after birth. The Late Total Parenteral Nutrition group (LTPN), started on a solution containing glucose during the first 48 hours of life, followed by 2 g/kilo-day of AA and 0.5 g/kilo-day of IL. For the LTPN group AA and IL were each increased by 0.5 g/kilo-day to a maximum of 3.5 and 3 g/kilo-day, respectively. RESULTS: Nitrogen retention was significantly greater in all infants in the ETPN group throughout the 7-day study period. All infants in the LTPN group were in negative nitrogen balance during the first 48 hours of life, while those in the ETPN group were in positive nitrogen balance throughout. The mean (+/-SD) nitrogen retention in the ETPN was 384.5 mg/kilo-day (+/-20.2), compared to 203.4 mg/kilo-day (+/-20.9) in the LTPN group (p <0.001). In each of the first 5 days of life, energy intake was significantly greater in the ETPN group compared to the LTPN group (p <0.001). Mean fluid intake during the study period was similar between, the ETPN and the LTPN groups (162 and 165 cm3/kilo-day, respectively). The mean weight gain was similar in the ETPN and LTPN groups. Plasma levels of cholesterol, triglycerides, bicarbonate, blood urea nitrogen, creatinine, and pH were similar in both groups during the study period. Mean (+/-SD) serum glucose in the LTPN group was higher, but remained in normal range (101.1+/-5.2 and 80.8+/-5.4 mg/kilo-day, respectively). The mean peak serum bilirubin was significantly higher in the ETPN group, compared to The LTPN group (7.7 and 6.2 mg/dl). CONCLUSION: This study shows that aggressive intake of AA and IL can be tolerated immediately after birth by VLBW infants. Also, ETPN significantly increased positive nitrogen balance and caloric intake, without increasing the risk of metabolic acidosis, hypercholesterolemia, or hypertriglyceridemia.

Amino Acids↗
PubMed1992

The sustained development of preneoplastic lesions depends on high protein intake.

The effects of sequential alterations in the feeding of two levels of dietary protein (5% and 20% casein) on the postinitiation development of aflatoxin B1- (AFB1) induced gamma-glutamyl transpeptidase-positive (GGT+) preneoplastic foci were examined. Weanling male Fischer 344 rats fed AIN-76A diet (20% protein) were administered 10 intragastric doses of AFB1 (1 dose/day during the 14-day dosing period excluding weekends) at 250 micrograms/kg body wt (initiation). After AFB1 tissue clearance, rats were randomly assigned to dietary treatment groups. During the next 12 weeks (promotion), they developed AFB1-induced GGT+ preneoplastic lesions. The 12-week promotion period was subdivided into four three-week periods, during which rats were fed isocaloric diets containing 20% casein during all four periods (20:20:20:20), 5% casein during all four periods (5:5:5:5), or sequentially altered casein levels (20:5:20:5 and 5:20:5:20). Rats were killed at 3,6,9, and 12 weeks to examine the dependence of GGT+ foci development on protein intake. Animals fed 5% casein diets developed significantly fewer (p < 0.01) GGT+ foci than animals fed 20% casein diets despite greater total caloric intake. Similarly, in the intervention groups, preneoplastic development was enhanced when the 20% casein diet was fed and inhibited when the 5% casein diet was fed. These results indicate that the sustained development of AFB1-induced preneoplastic foci depends on a high protein intake. Alternatively, these results suggest that low protein intake inhibits lesion development.

Aflatoxin B1↗
PubMed2006

Caloric restriction and aging: controversial issues.

It has long been held that food restriction extends the life span of rodents and other species by decreasing caloric intake and slowing the rate of aging. Recent findings challenge these concepts. This review assesses these controversial issues. The conclusion is that caloric restriction underlies the life extension of rats, but not of Drosophila. Mortality characteristics show that food restriction slows the rate of aging of rats and, in some studies, of mice. However, in other mouse studies and in Drosophila, mortality characteristics have been interpreted as indicating that it delays the start but does not slow the rate of aging; the author believes that this interpretation is faulty. These differences in mortality responses to food restriction provide a potentially powerful tool for uncovering basic mechanisms underlying its life-prolonging action. A hypothesis is presented for use in the search for these mechanisms.

Age Factors↗
PubMed2003

Mechanisms of dairy modulation of adiposity.

Dietary calcium plays a pivotal role in the regulation of energy metabolism, in that we have found high calcium diets to attenuate adipocyte lipid accretion and weight gain during periods of overconsumption of an energy-dense diet and to increase lipolysis and preserve thermogenesis during caloric restriction, thereby markedly accelerating weight loss. Our studies of the agouti gene in obesity and insulin resistance demonstrate a key role for intracellular Ca(2+) in regulating adipocyte lipid metabolism and triglyceride storage, with increased intracellular Ca(2+), resulting in stimulation of lipogenic gene expression and lipogenesis, and suppression of lipolysis, resulting in adipocyte lipid filling and increased adiposity. Moreover, we have recently demonstrated that the increased calcitriol produced in response to low calcium diets stimulates Ca(2+) influx in human adipocytes and thereby promotes adiposity. Accordingly, suppressing calcitriol levels by increasing dietary calcium is an attractive target for the prevention and management of obesity. In support of this concept, transgenic mice expressing the agouti gene specifically in adipocytes (a humanlike pattern) respond to low calcium diets with accelerated weight gain and fat accretion, whereas high calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis and suppress fat accretion and weight gain in animals maintained at identical caloric intakes. Further, low calcium diets impede body fat loss, whereas high calcium diets markedly accelerate fat loss in transgenic mice subjected to caloric restriction. Notably, dairy sources of calcium exert markedly greater effects in attenuating weight and fat gain and accelerating fat loss. This augmented effect of dairy vs. supplemental calcium is likely attributable to additional bioactive compounds in dairy that act synergistically with calcium to attenuate adiposity; among these are angiotensin converting enzyme inhibitory peptides, which limit angiotensin II production and thereby limit angiotensin II stimulation of adipocyte lipogenesis. These concepts are confirmed by both epidemiological and clinical data, which similarly demonstrate that dairy products exert a substantially greater effect on both fat loss and fat distribution compared to an equivalent amount of supplemental calcium.

Adipocytes↗
PubMed1993

Alterations in glucose metabolism in patients with Alzheimer's disease.

OBJECTIVE: To determine the alterations in glucose metabolism that occur in patients with Alzheimer's Disease (AD). DESIGN: Cross-sectional comparison of AD and healthy controls. SETTING: A University teaching hospital. PATIENTS: Healthy controls (n = 14, BMI: 24.9 +/- 0.5 kg/M2, age 73 +/- 1 years) and patients with AD (n = 12, BMI: 23.9 +/- 1.0 kg/M2, age 72 +/- 1 years). All controls and patients with AD had a normal history and physical examination, a negative family history of diabetes, and took no medications. MEASUREMENTS: All patients and controls underwent an assessment of their dietary intake and physical activity, a 3-hour oral glucose tolerance test (OGTT), and a 2-hour hyperglycemic glucose clamp study. RESULTS: Total caloric intake (AD: 27.1 +/- 1.3 kcal/kg/day; CONTROL: 23.6 +/- 1.6 kcal/kg/day; P = ns) and intake of complex carbohydrates (AD: 5.9 +/- 0.4 kcal/kg/day; CONTROL: 6.5 +/- 0.3 kcal/kg/day; P = ns) were not different between groups. Leisure time physical activity was greater in controls (AD: 2970 +/- 411 kcal/week; CONTROL: 5229 +/- 864 kcal/week; P < 0.05). Patients with AD had higher fasting glucose (AD: 5.9 +/- 0.2 mmol/L; CONTROL: 5.1 +/- 0.1 mmol/L; P < 0.01) and insulin (AD: 144 +/- 20 pmol/L; CONTROL: 100 +/- 6 pmol/L; P < 0.05) values. In response to the OGTT, the area under the curve for glucose and insulin was similar in both groups. During the hyperglycemic clamp, steady-state glucose values were higher in the Alzheimer's patients (AD: 11.5 +/- 0.2 mmol/L; CONTROL: 10.9 +/- 0.1 mmol/L, P < 0.01). First- and second-phase insulin responses were similar in each group. The insulin sensitivity index (units: mL/kg.min per pmol/L x 100), a measure of tissue sensitivity to insulin, was reduced in the patients with AD (AD: 0.59 +/- 0.06; CONTROL: 0.79 +/- 0.07; P < 0.05). CONCLUSIONS: We conclude that early AD is characterized by alterations in peripheral glucose metabolism, which may relate, in part, to alterations in physical activity.

Aged↗
PubMed2003

Lessons from experimental disruptions of the menstrual cycle in humans and monkeys.

Prospective studies in humans and monkeys have informed our understanding of the mechanism of exercise-associated menstrual disorders (EAMD). These studies have provided convincing evidence that a key causal factor in the development of EAMD is an imbalance between energy intake and energy expenditure. This imbalance is created by the increased energy cost of exercise in the face of inadequate supplementation of caloric intake. Although one prospective study in humans documents the impact of weight loss, studies in nonhuman primates (Macaca fasicularis) reveal that EAMD can occur with unobtrusive compensatory mechanisms indicative of energy conservation. The onset of EAMD is variable between individuals, but is abrupt, and with little forewarning with respect to recognizable symptoms. Future studies aimed at mechanisms should build upon the finding that key metabolic signals such as T3 are correlated with both the onset and reversal of EAMD, perhaps by focusing on concomitant metabolic changes that directly influence GnRH neurons. Translational studies examining the energetics of the reversal of EAMD by manipulating food intake and or exercise should build on the findings in the monkey model. Lastly, because EAMD is often associated with disordered eating, future prospective studies in humans should incorporate the potential interaction of disordered eating and psychosocial stress on EAMD.

Animals↗
PubMed1991

The Mechanism of Weight Loss after Ileo-gastrostomy for Morbid Obesity.

Twelve patients (weight 107-178 kg and age range 19-43 years) were investigated following ileo-gastrostomy for morbid obesity. A number of variables were studied prospectively, pre- and postoperatively, to determine the cause of weight loss-previously attributed to malabsorption or decreased caloric intake. Weight loss of 10.9-36.5 kg, mean 22.9 kg, occurred. Three-day calorie counts demonstrated a postoperative decrease in daily caloric consumption of 320-3870, mean 1975 cal. Analysis of body compartment composition after derivation of lean body mass (from calculation of total body water with tritiated water) showed a mean decrease in adipose tissue of 17.7 kg. Postoperative weight loss, mainly fat, could not all be accounted for by decreased caloric consumption or steatorrhea (72-h stool fat increased by a mean of 30 g). Pulmonary studies showed no significant change in respiratory quotient, but a large decrease in both postoperative utilization of oxygen and the production of carbon dioxide. This may indicate an alternate, anaerobic, energy cycle utilization. Other statistically significant variables included a large fall in cholesterol, LDH cholesterol and triglycerides, and smaller decrease in HDL cholesterol. Changes in gastro-intestinal (GI) hormones and cell counts in stomach and small intestine were also measured and will be reported later.

Journal Article↗
PubMed2005

[Nutritional assessment in patients with cirrhosis: the use of indirect calorimetry].

BACKGROUND: Malnutrition is frequent in cirrhotic patients, and its assessment is difficult. Functional assessment through a dynamometer is a simple method and could minimize these drawbacks. Harris-Benedict prediction formulae estimates the resting energy expenditure but has not been validated for this population. One alternative is the use of indirect calorimetry. AIM: To assess nutritional status in cirrhotic patients and estimates the resting energy expenditure through indirect calorimetry and compares it to Harris-Benedict. PATIENTS AND METHODS: Thirty four adult hepatitis C cirrhotic outpatients were studied, classified by Child-Pugh and model of end-stage liver disease score. The resting energy expenditure was predicted through Harris-Benedict and measured by indirect calorimetry. Nutritional assessment was done through anthropometry, subjective global assessment, hand-grip strength and a 3-day recall. RESULTS: Fifteen (44.2%) were Child-Pug A, 12 (35.3%) B and 7 (20.6%) C, and 33 (97.1%) had model of end-stage liver disease scores less than 20. The resting energy expenditure predicted was higher than the measured (Harris-Benedict 1404.5 +/- 150.3 kcal; indirect calorimetry 1059.9 +/- 309.6 kcal). The prevalence of malnutrition varied between methods (body mass index, muscle arm circumference, subjective global assessment, triceps skinfold thickness and hand-grip strength: 0; 5.9; 17.6; 35.3 and 79.4%, accordingly). Calories and proteins intake were 80% and 85% of recommended amounts and there was inadequate intake of calcium, magnesium, iron and zinc. CONCLUSION: Malnutrition was frequent and hand-grip strength seemed to be the most sensitive method for its diagnosis. Calories and protein intakes were inadequate. Considering that the predicted resting energy expenditure was higher than the measured one and the need to offer higher caloric intake, the use of the predicting equation may replace indirect calorimetry.

Adult↗
PubMed1980

Serum complement activity of protein-energy malnourished beef cows.

Beef heifers were fed protein- or energy-deficient rations (or both) for approximately the last 5 months of pregnancy. Serum samples were periodically collected and were analyzed for amounts of total complement (C) hemolytic activity. After being fed the rations for approximately 2 months, heifers given low-energy rations had significantly lower (P < 0.01) amounts of C than did those fed adequate energy rations, This decrease in C was observed regardless of the amount of dietary protein, although low protein intake seemed to exaggerate the effect of low energy consumption. Reduced protein in the rations had no effect on C titers when caloric intake was adequate. Also, the depressive effect of low dietary energy on C values was no longer apparent after approximately 4 months of feeding the rations. Amounts of C dropped by 20 to 40 U for all groups at or near the time of parturition. The C values averaged over all test dates were significantly lower (P < 0.05) for those heifers given low energy in their rations as compared with values for heifers fed adequate energy rations (146.9 vs 160.8 U).

Animals↗
PubMed2001

Glucose feeding exacerbates parathion-induced neurotoxicity.

Excessive dietary intake of sugars could alter various biotransformation processes and the pharmacological and toxicological properties of numerous xenobiotics. In the present study, the effects of glucose supplementation were examined on the neurotoxicity of the organophosphorus (OP) pesticide parathion (PS) and its active metabolite, paraoxon (PO), a potent inhibitor of acetylcholinesterase (AChE). Rats (n = 6-12/treatment group) were given free access to tap water or 15% glucose (w/v) in tap water beginning 7 d prior to OP toxicant exposure. Food, caloric intake, and body weight were measured daily. Animals were challenged with either PS (4.5, 9, or 18 mg/kg, sc) or PO (0.3 0.5, or 0.7 mg/kg, sc) and clinical signs of neurotoxicity (i.e., autonomic dysfunction, involuntary movements) were recorded daily for the following 13 d. Glucose feeding was associated with a dramatic drop (approximately 50%) in feed intake and an increase (approximately 20% in total caloric consumption over the 7 d prior to OP exposure. Functional toxicity associated with PS exposure was increased in glucose-fed (GF) rats, but the glucose diet had no apparent effect on clinical signs of toxicity following PO treatment. Glucose feeding increased the magnitude of AChE inhibition in the frontal cortex and plasma at lower dosages (i.e., 4.5 and 9 mg/kg) 3 d following PS treatment. Time-course studies (3, 7, and 11 d after PS exposure, 18 mg/kg, sc) indicated significantly greater brain and plasma AChE inhibition in glucose-fed animals at later time points. In contrast, glucose feeding had no effect on the degree of AChE inhibition following PO exposure. Neither liver microsomal oxidative desulfuration of PS, nor liver or plasma paraoxonase, nor liver or plasma carboxylesterase activities were measurably affected by glucose feeding. Downregulation of muscarinic receptors 7 d after PS exposure (18 mg/kg, sc) was more extensive in GF rats. It is postulated that excessiveglucose consumption decreases the intake of other dietary components, in particular amino acids, limiting the de novo synthesis of AChE and consequent recovery of synaptic transmission. Due to the shorter duration of inhibition following PO exposure, sponta neous reactivation of AChE may be more important than de novo protein synthesis in recovery of function, and thus with the effects of glucose feeding on its toxicity. Individuals that derive a large proportion of their calories from sugars may be at higher risk of acute toxicity from organophosphorus pesticides such as PS.

Animals↗