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Biomedical subjects

Z J Yang

Publications and source records attributed to Z J Yang.

At least 55 records · Page 3Linked to original sources

Temporal changes in meal number and meal size relationship in response to rHu IL-1 alpha.

Peripherally infused interleukin-1 reduces food intake. Its temporal and selective effects on meal number and meal size were investigated in seven rats continuously infused for 3 days with recombinant human interleukin-1 alpha (rHu IL-1 alpha; 3 micrograms day-1, i.v.). Food intake decreased significantly during the first two infusion days, and was brought about by first the early reduction of meal number, followed by meal size with a 1 day delay. The primary effect of rHu IL-1 alpha was seen during the dark cycle. After the infusion was stopped, meal number recovered most quickly, followed by a lag in recovery of meal size. We conclude that rHu IL-1 alpha influenced food intake primarily via an effect on meal number, which responds more rapidly than a decrease in meal size, thereby inducing an immediate decrease in food intake.

Animals↗

Hepatic vagus does not mediate IL-1 alpha induced anorexia.

Peripherally infused interleukin-alpha (IL-1 alpha) reduces food intake. Since the innervated liver modulates eating activity via the vagus, we investigated the role of the hepatic vagus in the etiology of IL-1 alpha induced anorexia. Ten male Fischer 344 rats were randomly assigned to hepatic vagotomy (HX-IL-1 group) or sham operation (Sham-IL-1 group), and an internal jugular catheter was inserted in all rats. Another six sham operated rats receiving normal saline i.v. throughout the study period served as general controls. After a 10-day recovery period, HX-IL-1 and Sham-ILI-1 rats were infused with 3 micrograms day-1 of IL-1 alpha for 3 days, followed by a 4 day infusion of saline. During the IL-1 alpha infusion, food intake was reduced at a similar rate and by a similar amount in both vagotomized and sham-operated rats. When IL-1 alpha infusion was stopped, food intake normalized at a similar rate in both HX-ILI-1 and Sham-IL-1 groups. These data indicate that the hepatic vagus is not involved in the etiology of IL-1 alpha induced anorexia.

Animals↗

LHA dopaminergic activity in obese and lean Zucker rats.

Microdialysis was performed to quantitate lateral hypothalamic dopamine (LHA DA) release before, during and after a single meal in food-deprived obese and lean Zucker rats to examine our hypothesis that an abnormally high dopamine activity may exist in the LHA of obese Zucker rats. Food consumption after food deprivation, was significantly greater in obese than in lean rats (4.1 +/- 0.2 and 2.3 +/- 0.4 g, respectively; (p < 0.05). Mean basal dopamine level was significantly higher in obese than in lean rats (12.0 +/- 0.3 and 10.5 +/- 0.3 pg in 10 microliters dialysates, respectively; p < 0.05). Dopamine release during eating was greater in obese than in lean rats (159.1 +/- 6.8% and 135.4 +/- 3.6% of baseline level, respectively; p < 0.05). After eating, the dopamine level returned to that before (105.6 +/- 4.5% in obese rats and 101.9 +/- 4.0% in lean rats) within the first 20 min sample. Data suggest that there may exist an inherently higher LHA DA 'threshold' level in obese Zucker rats and that until it is reached, food intake continues. This higher 'threshold' level may be responsible for their unique feeding behavior and is probably a contributory factor to their development of obesity.

Animals↗

Correlation between food intake and CSF IL-1 alpha in anorectic tumor bearing rats.

Postulating that central IL-1 is involved in the pathogenesis of cancer anorexia we measured IL-1 alpha in cerebrospinal fluid (CSF) from anorectic tumor bearing (TB) rats and non-tumor bearing controls, and correlated their CSF IL-1 alpha with food intake and tumor weight. Food intake in controls was significantly higher than that in anorectic TB rats. Eight of the 13 anorectic TB rats had detectable CSF IL-1 alpha; no CSF IL-1 alpha was detected in controls. In anorectic TB rats a negative correlation existed between CSF IL-1 alpha and food intake and a positive correlation between CSF IL-1 alpha and tumor weight. Data suggest a link between CSF IL-1 alpha and the pathogenesis of cancer anorexia.

Animals↗

Effects of TPN on brain, liver, and food intake in rats.

Postulating that total parenteral nutrition (TPN) has a direct metabolic effect in the brain which may be similar to that in the liver, we studied the effects of TPN on brain glycogen and triglyceride in rats. Control rats (n = 24) received normal saline via jugular catheter for 18 days; TPN rats (n = 24) had normal saline for 10 days and then TPN-100 for 4 days, followed by normal saline for 4 more days. TPN-100 (caloric ratio glucose: fat:amino acid = 50:30:20) provided 100% of the rat's daily caloric needs. Chow and water were available ad libitum during the study. Eight rats from each group were sacrificed after 1 and 4 days of TPN-100, and 4 days after stopping TPN-100. Glycogen in brain and liver glycogen, triglyceride, and glycogen synthetase and phosphorylase were measured, as were plasma glucose and insulin. Data were evaluated using Student's t test. With TPN, the following occurred: (a) an 85% decrease (P < 0.05) of spontaneous food intake; (b) an elevated plasma glucose; (c) a three- to fivefold increase (P < 0.01) in plasma insulin; (d) a 23% increase (P < 0.05) in whole brain glycogen but a 22-33% decrease (P < 0.05) in liver glycogen; (e) liver glycogen synthetase and phosphorylase activity were unchanged while whole brain glycogen synthetase activity decreased by 27% (P < 0.05) and phosphorylase activity increased by 10-16%; and (f) whole brain triglyceride content did not change, although there was a 155-241% increase (P < 0.01) in liver triglyceride.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of different types of isocaloric parenteral nutrients on food intake and metabolic concomitants.

Whether spontaneous food intake (SFI) is controlled by infused nutrient type or its caloric content, irrespective of nutrient type, was investigated. Rats were infused for 4 days with isocaloric solutions of different nutrient type but sharing the same intermediary metabolic oxidative pathway, providing 25% of daily caloric needs. One parenteral solution was a glucose, fat and amino acid mix (TPN-25%); the other provided ketone bodies (TRI-3.5%). Effects of parenteral infusions on SFI and metabolic concomitants were compared and contrasted to that in a group of orally fed rats. Both infusions reduced SFT by 50%. Rats receiving TRI-3.5% had lower blood glucose and insulin concentrations, but increased hepatic glycogen content compared to TPN-25% or orally fed rats. No differences in hepatic triglycerides occurred between the three groups. However, serum free fatty acids were significantly lower in TRI-3.5% and in TPN-25% groups vs. fed rats. Data indicate food intake suppression is mediated by caloric content rather than nutrient type, suggesting that a mediator of SFI regulation could be at the citric acid cycle level.

Amino Acids↗

Effects of fasting, intermittent feeding, or continuous parenteral nutrition on rat liver and brain energy metabolism as assessed by 31P-NMR.

We wanted to determine what happens to brain PCr and ATP relative to that in liver during a series of dietary manipulation consisting of a severe fast, during eating (when nutrients are intermittently supplied), and during and after PN-100, when an excess amount of nutrients are continuously supplied, using 31P-NMR spectroscopy, in rats randomized to a Fast or Fed group in which energy was provided either as chow or as PN-100. Liver ATP concentration, and brain and liver 31P-nuclear magnetic resonance (NMR) spectras were measured serially. Brain energy metabolism was not different between groups and among days. In contrast, Fasted group showed increased liver ATP/Pi ratio and decreased ATP concentration and ATP/phosphomonoester ratio, there being no difference between Fed and PN-100 groups. Data suggest that brain energy metabolism is maintained regardless of whether energy is supplied intermittently or continuously, and during a negative caloric intake period, brain energy metabolism is quantitatively preserved, suggesting that ATP production by liver is subservient to brain ATP state.

Adenosine Triphosphate↗

Continuous systemic interleukin-1 alpha infusion suppresses food intake without increasing lateral hypothalamic dopamine activity.

In addition to its immunomodulatory action, interleukin-1 (IL-1 alpha) induces anorexia centrally. Whether IL-1-induced anorexia is mediated by dopaminergic activity in the lateral hypothalamic area (LHA) was investigated by using microdialysis in freely moving rats. After recovery from jugular vein catheterization and LHA cannulation, rats had a microdialysis probe inserted into the LHA. Microdialysis samples were continuously collected in control rats not infused, and in IL-1-treated rats during and after a 24 h continuous systemic infusion of 6 micrograms IL-1 alpha. IL-1 alpha significantly suppressed food intake from 13.6 +/- 0.1 g to 4.3 +/- 0.8 g (p < 0.001), but there was no significant difference in dopamine concentration in the LHA dialysates before, during and after IL-1 alpha infusion relative to controls. Although IL-1 alpha has been shown to act centrally, our results suggest that the anorexic effect of IL-1 alpha is not mediated through dopaminergic activity in the LHA.

Animals↗

Eating induced rise in LHA-dopamine correlates with meal size in normal and bulbectomized rats.

Dopaminergic function in the lateral hypothalamic area (LHA) is important for processing intrinsic and extrinsic feeding related information. Brain microdialysis was used to examine if dopamine release in the LHA correlates with meal size in normal and bulbectomized rats. Food-deprived bulbectomized rats ate significantly less food (1.7 +/- 0.1 g) than food-deprived sham operated rats (3.1 +/- 0.5 g, p < 0.05), accompanied by a lesser increase in LHA-dopamine release (150.6 +/- 4.9% vs. 195.1 +/- 13.9, p < 0.02). LHA-dopamine release was significantly higher in rats which ate a full meal (2.9 +/- 0.1 g) than in rats which ate half a meal (1.5 +/- 0.1 g, p < 0.05), being 155.9 +/- 7.8% vs. 131.0 +/- 4.9% (p < 0.05) in food-deprived normal rats. Data suggest that dopamine release in the LHA correlates to the quantity of food consumed during a meal.

Animals↗

Tumor necrosis factor-alpha and total parenteral nutrition-induced anorexia.

BACKGROUND: We hypothesize that total parenteral nutrition (TPN) induces anorexia by an increase in anorexigenic cytokines (factors with central action via the hypothalamus) and tested this hypothesis by measuring changes in food intake and cytokines in response to TPN. METHODS: Fischer rats with an internal jugular catheter and ad libitum food received saline solution for 10 days. On day 11, rats were randomized to TPN (G:F:AA = 50:30:20) for 4 days (days 11 through 14); control rats received on saline solution for 5 days. On day 14, one half of the TPN group was switched back to saline solution for 1 day. Daily food intake was measured. On day 14 in one half of all rats and on day 15 in the remaining, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 alpha were measured in plasma and cerebrospinal fluid (CSF). Spontaneous in vitro TNF-alpha and IL-1 alpha were also measured in peripheral blood mononuclear cells. RESULTS: With TPN, an 80% decrease (p < 0.01) in food intake occurred; plasma TNF-alpha increased (78 +/- 9 pg/ml vs undetectable; p < 0.001), and IL-1 alpha was undetectable. Spontaneous in vitro TNF-alpha and IL-1 alpha production were unchanged. Stoppage of TPN led to return toward normal of food intake and plasma TNF-alpha. TNF-alpha and IL-1 alpha in CSF were undetectable in both groups during and after TPN. CONCLUSION: Increase in plasma TNF-alpha with no increase in CSF-TNF-alpha during TPN, when food intake decreased, suggests an association between TPN and TNF-alpha but not necessarily cause and effect.

Animals↗

The prediction of fetal acidosis at birth by computerised analysis of intrapartum cardiotocography.

OBJECTIVE: To assess the capability of a computer software interpretation program, using intrapartum fetal heart rate and intrauterine pressure as recorded in a cardiotocogram to predict fetal acidosis at birth. DESIGN AND SUBJECTS: A retrospective analysis of digitised fetal heart rate and uterine activity values obtained from 73 high risk women in labour. SETTING: Two university teaching hospitals. METHODS: A computer software program was constructed to analyse the digitised data and predict acidosis. The results of the analysis were compared with actual umbilical arterial blood pH and base excess at delivery. RESULTS: The software cardiotocogram interpreter was able to predict a pH of less than 7.15 with an accuracy of 77%, a sensitivity of 88% and specificity of 75% in this set of data. It was able to predict a base excess of less than -8 mmol/l with an accuracy of 81%, a sensitivity of 76% and specificity of 82%. CONCLUSIONS: A computerised method of analysing fetal heart rate and uterine activity using a simple algorithm has demonstrated a capability to predict fetal acidosis at the time of delivery. Further research in this area is warranted.

Acidosis↗

[Preliminary study on relationship between syndrome differentiation of esophageal cancer and changes of exfoliated cells of tongue coating].

Exfoliated cells of tongue coating of 63 esophageal cancer (EC) cases have been investigated by applying exfoliate cytologic examination, which showed that abnormal cornified cells were commonly seen while they were less in the patients of EC than those in the healthy group, and their difference was significant (P < 0.05), It showed an increase mainly in the number of pro-cornified cells in the patient of the Qi-Yang Deficiency group, an increase mainly in completely cornified cells in the Yin Deficiency and an increase in both pro-cornified cells and completely cornified cells in Phlegn-Dampness and blood Stasis patients. The difference among four groups was significant (P < 0.05). The changes of exfoliated cells of tongue coating provided an objective index for the early diagnosis of EC.

Adenocarcinoma↗

Metabolic influences on satiety in rats receiving parenteral nutrition.

Food intake is reduced during parenteral nutrition (PN) proportionally to the amount of calories or composition of the solution infused. The relative importance of infused glucose and lipid, 50 and 30% of PN kilocalories, respectively, in reducing food intake during PN was examined. Glycolysis, fatty acid oxidation, or both were acutely disrupted with 2-deoxy-D-glucose (2-DG) and mercaptoacetate (MA). Rats receiving intravenous infusions of saline or a PN solution providing 100% of total daily calories (PN-100) received a single intraperitoneal injection of saline, 2-DG, and/or MA during the early light phase. 2-DG (1.4 or 2.2 mmol/kg) did not initiate feeding in PN-100 rats, although hyperglycemia was evident in all rats 1 h after 2-DG. Food intake of PN-100 rats after MA (0.4 mmol/kg) was approximately 50% that of control rats. When 2-DG (1.4 mmol/kg) and MA (0.4 mmol/kg) were administered concomitantly, PN-100 and control rats consumed the same amount of food. During PN-100, rats appeared to be more sensitive to losing metabolic energy derived from lipid than from glucose.

Animals↗

Hepatic vagotomy effects on metabolic challenges during parenteral nutrition in rats.

During parenteral nutrition (PN) glucoprivic-induced feeding appeared to be neutralized by the oxidation of infused fatty acids. With the use of a latin-square design, the feeding response to 2-deoxy-D-glucose (2-DG) and/or 2-mercaptoacetate (MA) was evaluated in male Sprague-Dawley rats with hepatic branch vagotomy (HV) or sham operations (SO). Rats received continuous infusions of 0.9% saline or PN providing 100% of daily caloric needs (PN-100) for four consecutive days. During PN-100, food intake was stimulated by 2-DG in HV rats and when fatty acid oxidation was simultaneously inhibited by MA. 2-DG-induced hyperglycemia was apparent under all conditions. Lipoprivic-induced feeding and increased plasma free fatty acid concentrations were absent in HV rats, whether MA was administered alone or with 2-DG. The feeding response to glucoprivic challenges is influenced by the relative availability of alternate energy sources. The lack of feeding response to 2-DG during PN-100 is mediated by vagal input of hepatic fatty acid oxidation status.

Animals↗

Factors influencing compensatory feeding during parenteral nutrition in rats.

During parenteral nutrition (PN) there is an incomplete compensatory decrease in oral caloric intake. The effects of two factors influencing nutrient utilization, diurnal timing of PN infusion and composition of available diet, on compensatory feeding were investigated in male rats receiving 100% of daily caloric need as PN (PN-100). Compensation for infused calories increased from 70 to 80% (P < 0.05) when the timing of infused kilocalories more closely matched diurnal pattern of oral kilocalories intake (e.g., 75% kcal daily during the dark phase, 25% during the light phase). There was a similar degree of compensation when the diet and PN-100 had the same caloric distribution (50% kcal from carbohydrate, 30% from fat, and 20% from protein). Adjusting the diurnal timing of infused calories and diet composition concurrently further increased compensation for infused calories from 70 to 90% (P < 0.05). In the rat PN-100 model, compensation for infused calories is improved by adjusting the temporal pattern of infusions and diet composition.

Adaptation, Physiological↗

Synergistic effect of rhTNF-alpha and rhIL-1 alpha in inducing anorexia in rats.

To investigate whether there is a synergistic effect of recombinant human tumor necrosis factor-alpha (rhTNF-alpha) and recombinant human interleukin-1 alpha (rhIL-1 alpha) in inducing anorexia, 32 rats with jugular catheters were studied (8 rats/group): controls received normal saline; the IL-1 group received rhIL-1 alpha (10 micrograms/kg); the TNF group received rhTNF-alpha (30 micrograms/kg); and the IL-1 + TNF group received the same concentration of both rhIL-1 alpha+rhTNF-alpha for 3 days; solutions were then switched to normal saline. No significant decrease in light- and dark-phase food intake occurred during infusion of subeffective rhTNF-alpha. Food intake was decreased on the first rhIL-1 alpha infusion day because of a decreased meal number during the dark phase. A significant decrease in food intake occurred with combined infusion of rhIL-1 alpha+rhTNF-alpha because of a reduction in meal number during dark phase and meal size during light phase. Our results show that rhIL-1 alpha and rhTNF-alpha, when administered concurrently, had a synergistic effect in inducing anorexia, suggesting that low concentrations of these cytokines as produced endogenously may have potential effects on other biological functions in vivo.

Animals↗

Olfactory bulbectomy in rats modulates feeding pattern but not total food intake.

The role of olfactory input in the regulation of food intake and feeding patterns in rats was investigated by performing bilateral olfactory bulbectomy. Compared to control rats, bulbectomized rats ate the same amounts of food, but did so via a decrease in meal size, and a doubling in meal number. Although no increase in meal duration occurred, the exploratory behavior of sniffing during meals and between meals also increased significantly. While it is not yet clear how the olfactory bulbs participate in regulating food intake configuration resulting in changed feeding patterns, their clinical role can be appreciated by observing the acute changes in feeding pattern that occur when their input to the lateral hypothalamic area is damaged experimentally.

Animals↗