Biomedical subjects

Z J Yang

Publications and source records attributed to Z J Yang.

At least 37 records · Page 2Linked to original sources

PubMed1997

Acute adaptive changes in food intake pattern following olfactory ablation in rats.

We determined whether acute compensatory feeding pattern changes after bulbectomy persist on a chronic basis, or whether physiological adaptation occurs to normalize acute changes. Rats were randomized to olfactory bulbectomy or sham operation; all had jugular vein catheterization. Food intake, meal number and size were studied during infusion of parenteral nutrients providing 100% daily caloric intake (PN-100) to minimize post-ingestive effects. Rats were randomly assigned to acute (from day 14 after operation, PN-100 infused for 4 days, followed by 4 days of saline infusion) or chronic study (PN-100 infused for 4 days from day 40, followed by 4 days of saline infusion). After olfactory ablation, acutely decreased meal size was offset by increased meal number, but 40 days after, baseline differences between meal size and number no longer existed. No qualitative differences in response to PN-100 were noted between acute and chronic groups. Findings suggest a functional adaptation of food intake regulatory mechanism between 14 and 40 days after bulbectomy.

Adaptation, Psychological↗

PubMed1997

Eating-associated VMN-dopamine levels of rats: comparison of oral and intragastric feeding.

Eating is associated with persistently low dopamine (DA) concentration in the ventromedial hypothalamic nucleus (VMN), postulated to influence postprandial satiety. Whether pregastric factors contribute to eating-associated low VMN-DA was examined. VMN-DA levels were continuously measured in awake rats, food-deprived for 24 h, and either subsequently allowed to eat solid chow freely available for 20 min, an oral liquid diet, or an isovolemic isocaloric liquid diet infused intragastrically to bypass the oropharynx. Eating either solid chow or a liquid diet was associated with an immediate decrease in VMN-DA concentration. The lower VMN-DA concentration lasted longer after solid chow was consumed than following consumption of the liquid diet. When the oropharynx was bypassed no significant change in VMN-DA concentration was observed either during or after the liquid diet was infused. Results suggest that pregastric oropharyngeal factors contribute to eating-associated low VMN-DA concentration.

Administration, Oral↗

PubMed1997

Meal-induced changes in hepatic glycogen of fasted rats.

Hepatic metabolism of glucose and other nutrients influences feeding behavior. The present study was conducted to confirm prandial decreases in hepatic glycogen concentrations following a short-term fast. Male Sprague-Dawley rats were fasted 6-12 h during the light phase before having access to chow for one or two 20-min meals at the beginning of the dark phase. Plasma glucose and insulin concentrations in hepatic and portal venous blood and hepatic glycogen concentrations prior to and at the end of each meal were compared. Glucose concentration in the hepatic vein was greater than that in the portal vein prior to the meals but not at the end of the meal. Insulin levels were higher in the portal vein than the hepatic vein pre- and postprandially. Hepatic glycogen concentrations increased after each meal in younger (2-month-old) rats but not older (6-month-old) rats. Fasting levels of hepatic glycogen were lower in the younger rats than the older rats; however, the increase in hepatic glycogen was not due to differences in baseline glycogen concentrations at the start of the meal. The reported prandial decreases in hepatic glycogen of fasted rats were not apparent in this study. Because of the difference between 2- and 6-month-old rats in periprandial hepatic glycogen metabolism after a short-term fast, the age of the animal needs to be considered if the dynamics of liver glycogen metabolism are to be incorporated into a model of food intake regulation.

Age Factors↗

PubMed1997

Bilateral hypothalamic dopamine infusion in male Zucker rat suppresses feeding due to reduced meal size.

Lateral hypothalamic area dopamine activity (LHA-DA) appears to play a contributory role in regulating food intake, in particular, meal size. In this study we examined our hypothesis that bilateral LHA-DA injection induced depression of food intake via reduced meal size. Dopamine (11 mg/ml) or vehicle was infused into bilateral LHA at 0.5 microliter/h via two osmotic minipumps in six study or six control obese male Zucker rats for 13 days, respectively. Meal size, meal number, as well as food intake were continuously measured before, during, and after dopamine infusion. Intra-LHA-DA infusion significantly depressed food intake. The decreased food intake was solely caused by a significant and profound reduction in meal size. There was a modest compensatory rise in meal number that gradually increased food intake so that it reached control level on 10th dopamine infusion day. However, feeding pattern did not normalize until dopamine infusion ceased. The findings support our hypothesis that LHA-DA may participate in regulating meal size. Data also demonstrate that meal size and meal number are regulated in a reciprocal and independent manner to compensate for each other.

Animals↗

PubMed1997

Osteogenic responses to extraskeletally implanted synthetic porous calcium phosphate ceramics: an early stage histomorphological study in dogs.

In this experiment, synthetic porous calcium phosphate ceramics (hydroxyapatite-tricalcium phosphate) were prepared and implanted in dorsal muscles of dogs. The purpose was to study the biological processes prior to and during the morphogenesis of bone in extraskeletally implanted porous calcium phosphate ceramics. Specimens were harvested after implantation for 7, 15, 30, 45, 60, 90 and 120 days. Decalcified and undecalcified sections were prepared for alkaline phosphatase (ALP) histochemical localization and comparative histological analysis. The results show that bone morphogenesis in the pore regions of the extraskeletally implanted ceramics follows a complex process involving clot formation, vascular invasion, granulation-like tissue formation, polymorphic cell aggregation, osteoblast differentiation and bone formation. The characteristic feature preceding bone formation was polymorphic cell aggregation on the pore inner surface and near the invading capillaries or small venules. These cells were of various sizes and shapes, and some of them were positive for ALP activity. ALP-positive cell aggregates were more numerous where capillaries or venules were close to the pore inner surface. Osteoblast differentiation occurred within the cell clusters aggregated on the pore inner surface and bone matrix was secreted in direct contact with the ceramics. During bone formation, capillaries or small venules were always found close to the developing fronts of the osseous nidi. It is suggested that those cells which first appeared near the invading vasculature, the cells which aggregated on the pore inner surface and those cells which finally differentiated into osteoblasts may be interrelated in some way.

Journal Article↗

PubMed1997

Meal size and number: relationship to dopamine levels in the ventromedial hypothalamic nucleus.

Evidence shows a reciprocal relationship exists between the lateral hypothalamic area (LHA) and the ventromedial hypothalamic nucleus (VMN) in food intake regulation. Since a direct correlation between meal size and LHA-dopamine in Fischer rats was previously reported, we tested the hypothesis that an inverse association may exist between meal size and VMN-dopamine response. This was studied in awake 24-h food-deprived rats who were then allowed to eat freely for 20 min while the VMN-dopamine response was measured by microdialysis every 20 min for 2 h. In a second experiment, only one-half the amount freely eaten was provided during microdialysis. The following were observed. 1) Dopamine concentrations in VMN decreased during eating. 2) The degree and duration of decrease after the meal corresponded to the size of the meal. 3) When the decreased postmeal VMN-dopamine level had returned to baseline and food was available, rats ate once more. The findings show that, in normal rats, eating was associated with decreased dopamine levels in the VMN and was followed by a lag time during which no additional eating occurred. VMN dopamine levels thereby contribute to determining the duration of the intermeal interval and hence, by inference, the meal number.

Animals↗

PubMed1996

Mechanism of early tumor anorexia.

Whether in tumor-bearing rats a temporal relationship exists between an increase in plasma free tryptophan (FTRP), an increase in brain serotonin (5-HT), and onset of anorexia was studied. Rats were assigned to three groups: tumor-bearing (TB), pair fed (PF), and controls. Food intake was recorded daily. In TB rats anorexia developed on Day 18 and thereafter food intake decreased progressively until end of study. After tumor inoculation, tumor became palpable on Day 10 and continued to grow exponentially until end of study. Rats were killed on Days 6, 10, 16, 18, 22, and 26 to determine plasma FTRP, FTRP/LNAA, and brain 5HT and compared to PF and controls. On Day 6, before tumors became detectable, FTRP and FTRP/LNAA were increased (P < 0.05) in TB rats vs controls. Both continued to increase so that by Day 18 when food intake had started to decrease (P < 0.05), brain 5-HT increased and correlated with the onset of anorexia (R2 = 0.6, P < 0.05). Increases in plasma FTRP the precursor to brain 5-HT occurred in TB rats before physical appearance of tumor and increased until an increase in brain 5-HT occurred, leading to anorexia.

Amino Acids↗

PubMed1996

Increased food intake and body weight gain after lateral hypothalamic dopaminergic cell implantation.

To examine our hypothesis that dopamine activity in the lateral hypothalamic area (LHA) may play a role in enhancing the process of eating, a fetal cell suspension of predominantly dopaminergic cells was bilaterally transplanted into the LHA of study rats via direct injection; controls had carrier medium injection. Thereafter, mean daily food intake was 1 g per day greater in dopaminergic cell transplanted rats vs. controls for each day of the 10-week observation period. This resulted in a significantly greater cumulative body weight gain in study rats vs. controls (386 +/- 5.1 g vs. 354 +/- 3.8 g, respectively). On sacrifice at the end of the study, transplanted cells in the LHA were viable. Our data suggest that bilateral LHA dopaminergic cell transplant which presumably resulted in chronically and persistently enhanced dopaminergic activity in the LHA is associated with overeating and consequently, an excess weight gain.

Animals↗

PubMed1996

Carnitine supplementation accelerates normalization of food intake depressed during TPN.

When total parenteral nutrition (TPN; containing glucose, fat, and amino acids; caloric ratio 50:30:20) providing 100% of the rat's daily caloric intake is given for 3-4 days, food intake rapidly decreases by approximately 85%. After stopping TPN, there is a lag period of 3-4 days before food intake returns to previous level, which appears to be related to fatty acid oxidation and fat deposition. Carnitine plays a key role in the oxidation of fatty acids, and was demonstrated to reduce fat deposition in rats receiving TPN, by increasing beta oxidation. We therefore investigated whether rats receiving TPN supplemented with carnitine may prevent either the decrease or speed up the resumption or normalization of food intake, after TPN is stopped. Fourteen adult Fischer-344 rats had a central venous catheter inserted. After 10 recovery days, controls (n = 7) were infused with TPN providing 100% of rat's daily caloric intake for 3 consecutive days, followed by 4 more days of normal saline. The carnitine group (n = 7) received the same solution, but which provided 100 mg/kg/day carnitine. Daily food intake was measured and data were analyzed using ANOVA and Student's t-test. Both parenteral solutions depressed food intake maximally by almost 90% by day 3. Carnitine accelerated the normalization of food intake by decreasing the lag period by 1 day. We conclude that the addition of carnitine enhanced the normalization of post-TPN food intake and argue that this may be on the basis of enhanced fatty acid oxidation, a substrate known to play a significant role in the anorexia induced by TPN.

Animals↗

PubMed1996

Studies on the regulation of food intake using rat total parenteral nutrition as a model.

Total parenteral nutrition (TPN) is essential for maintaining the nutritional status of patients who are unable to eat sufficiently to meet their metabolic needs. However, TPN suppresses appetite and ultimately diminishes food intake. Theories concerning the role(s) of peripheral metabolites as signals, acting via the liver and the hypothalamus, for the metabolic control of food intake, have been put forward to explain the anorectic effect of TPN. In addition, it is postulated that changes in peripheral metabolites during TPN may be translated into changes in the levels of brain neurotransmitters known to decrease food intake. This review summarizes studies concerning the effect of TPN on food intake. These studies have involved: (1) characterizing the changes in feeding activity due to TPN; (2) investigating the involvement of the central nervous system; and (3) investigating the role of the periphery and its metabolites in the regulation of food intake during TPN. Some insight into the mechanism of action of TPN on food intake is provided.

Animals↗

PubMed1996

The gut-brain brain-gut axis in anorexia: toward an understanding of food intake regulation.

Our long-term objectives continue to be elucidation of the mechanisms that control spontaneous food intake (SFI), so that we may utilize this information in seeking ways to ameliorate abnormalities of SFI that occur in nutritionally ill humans. To this end, we have developed and used an Automated Computerized Rat Eater Meter (ACREM), which allows detailed determinations of food intake and feeding patterns under a wide variety of experimental conditions. Because food intake is the product of meal number and meal size, these indexes were studied in a variety of experimental situations: normal male Fischer rats, genetically obese Zucker rats, cancer-bearing rats, and an inflammatory bowel rat model. In each model, a reduction in food intake was accomplished; usually by a selective reduction in meal number and, occasionally, meal size; often in both. The independent regulation of meal number and meal size strongly suggests the existence of focal neuronal areas in the hypothalamic food regulatory areas of the brain, which independently control these feeding indexes. To these feeding pattern studies were added in vivo focal hypothalamic microdialysis to correlate changes in meal size and number with changes in the basic neurotransmitters, dopamine and serotonin. To further gain an understanding of anorexia and food intake regulation in these models as it relates to the brain and gut interaction, we used metabolic stimulants, anatomic ablation, and electrophysiological studies, cytokines, selective neurotransmitter agonists, and antagonists peripherally in the gut and centrally in the brain. An integrated view of the gut-brain brain-gut control of food intake has emerged as a working and testable model system. The system includes oronasal pregastric factors, which stimulate an increase in LHA-dopamine facilitating gastric compliance via efferent vagal fibers; postabsorptive factors, including nutrients and hepatoportal receptors via afferent vagal fibers that inhibit further LHA-dopamine, thereby regulating meal size. The same postabsorptive factors simultaneously decrease VMH-dopamine, thereby determining postprandial intermeal duration, because food intake is resumed when VMH-dopamine normalizes--thus regulating meal number. Changes in plasma amino acids, the precursors for neurotransmitters, also affect brain availability for neurotransmitters. This in particular applies to tryptophan, the precursor of serotonin in the VMH, which induces a decrease in meal number and cytokines, which facilitate activity of both dopamine and serotonin.

Animals↗

PubMed1996

From laboratory to bedside: new strategies in the treatment of malnutrition in cancer patients.

The objective of this review is to present and discuss the current and the possible future perspectives of artificial nutrition in preventing and treating cancer cachexia. English-language studies published in the last 25 years were retrieved using MEDLINE, bibliographies and consultation with experts. MEDLINE search terms included "cancer," "malnutrition," and "nutritional support." In vivo and in vitro controlled studies were selected, and data from each study were independently abstracted by the authors. Data obtained indicate that cancer cachexia is a common manifestation of advanced malignant disease, characterized by marasmus due to impaired nutrient metabolism, weight loss, and anemia. In patients, the presence of cachexia increases morbidity and mortality, delays or impedes the delivery of the adequate treatment, reduces the efficacy of anti-neoplastic therapy, and impairs patient's quality of life. Indirect evidence indicates that cancer cachexia is mediated by circulating cytokines, produced by the host in response to the presence of the malignancy. In the past two decades, nutritional support was used to counteract the detrimental effect of cancer cachexia on the host, but with limited success. More recently, the better understanding of the mechanisms of cancer cachexia and the identification of pharmacologic effects provided by specific nutrients, has formed the rationale for a "new" mode of nutrition therapy/nutritional support, adding pharmacotherapy to adjunctive initial care.

Cachexia↗

PubMed1996

Innervated liver plays an inhibitory role in regulation of food intake.

BACKGROUND: With the onset of eating, the associated rise of dopamine in the lateral hypothalamus (LHA-DA) is thought to regulate quantity of food consumed per meal. Early release of LHA-DA induced by eating is facilitated by oronasal stimulation; we propose that the subsequent LHA-DA response induced by nutrients in the portal vein is dampened by the innervated liver. This was tested by measuring LHA-DA in normal rats: during parenteral feeding to bypass oronasal stimulation, while eating during parenteral feeding, and while eating only. METHODS: Rats had either total liver denervation or sham operation, with placement of a jugular vein catheter and LHA-DA microdialysis cannula. After a 3-week recovery period total liver denervated rats were randomized to parenterally fed, food only, and parenteral plus food groups each with sham-operated controls in which LHA-DA was measured. RESULTS: No difference in LHA-DA release in food only groups occurred between total liver denervated or sham-operated rats. A significantly higher rise in LHA-DA was observed in total liver denervated versus sham-operated rats in parenterally fed (129% +/- 4% versus 116% +/- 2%; p < 0.05) and parenteral plus food (151% +/- 4% versus 134% +/- 4%; p < 0.05) groups. CONCLUSIONS: In total liver denervation versus sham operation, an increase in LHA-DA release occurs during parenteral feeding and eating during parenteral feeding, suggesting that innervated liver inhibits LHA-DA release.

Animals↗

PubMed1996

Cracking the riddle of cancer anorexia.

During tumor growth, anorexia and reduced food intake are among the major causes leading to malnutrition and eventually cachexia, which negatively affect patients' outcome. Consistent evidence from our laboratories in rats and humans indicates a key role for ventromedial hypothalamic (VMH) serotonergic system in the development of cancer anorexia. Thus, we postulated that during cancer, increased plasma tryptophan levels (the precursor of serotonin) lead to increased cerebrospinal fluid tryptophan concentrations and increased VMH serotonin synthesis, which then mediates the occurrence of anorexia. However, recent data strongly suggest that factors other than tryptophan supplied to the central nervous system might be involved in the pathogenesis of reduced food intake during tumor growth. Particularly, a significant role appears to be played by interleukin-1 (IL-1). We recently showed that IL-1 infusion in normal rats causes changes in food intake and its determinants, meal number and meal size, similar to those characterizing cancer anorexia, thus supporting the involvement of this cytokine in the development of anorexia. Interestingly, IL-1 and the VMH serotonergic system appear to be closely linked: peripherally infused IL-1 increases brain tryptophan and serotonin concentrations, while intracerebrally infused IL-1 increases neuronal firing rate and serotonin release. We therefore hypothesize that during tumor growth, increased production/secretion of IL-1 occurs, which facilitates the tryptophan supply to the brain. IL-1 can then also act on the VHM itself, where IL-1 receptors exist, to increase its neuronal activity and serotonin release. In other words, we believe that centrally acting IL-1 increases hypothalamic neuronal firing rate and serotonin release, while peripherally acting IL-1 is critical in supplying the hypothalamus with the precursor, tryptophan, in order to maintain the high rate of serotonin synthesis. Also, additional factors recently proposed as mediators of anorexia (including neuropeptide Y and nitric oxide) appear to be part of the hypothesized pathogenic mechanism.

Animals↗

PubMed1996

Eating-related increase of dopamine concentration in the LHA with oronasal stimulation.

Previously, we showed that eating was associated with an increase in lateral hypothalamic area dopamine (LHA-DA) release, which returns to previous level when eating stops. We therefore hypothesize that LHA-DA release may be primarily contributed to by oronasal stimulation. To test our hypothesis, microdialysis was used to compare LHA-DA release during oral and intragastric feeding. A gastrostomy tube was inserted in 12 rats. After recovery from surgery, in vivo microdialysis was performed. Six rats were allowed to drink a liquid diet, whereas in another six rats the same liquid diet was infused at paired doses (volume = 4.8 +/- 0.6 ml; time = 5-10 min) through the gastrostomy tube into the stomach. Oral feeding increased baseline LHA-DA from 10.6 +/- 0.2 to 14.0 +/- 0.8 pg/10 microliters dialysate (P < 0.01) within 20 min. No significant change in measured LHA-DA occurred during intragastric feeding [baseline: 10.5 +/- 0.3 pg/10 microliters; postintragastric: 10.2 +/- 0.3 pg/10 microliters (P < 0.01 vs. oral feeding)], indicating that LHA-DA release occurs with oronasal stimulation.

Administration, Oral↗

PubMed1996

Comparison of long-term feeding pattern between male and female Fischer 344 rats: influence of estrous cycle.

We studied the effect of gender on food intake, meal number, and meal size in eight 10-wk-old female and seven age-matched male Fischer 344 rats for 44 consecutive days. Although food intake (g/100 g body wt) was similar in males and females (5.42 +/- 0.10 vs. 5.13 +/- 0.13 g food.day-1.100 g body wt-1, respectively; not significant), weight gain in males was approximately seven times greater than in female rats (1.49 +/- 0.07 vs. 0.21 +/- 0.03 g/day, respectively; P < 0.001). During this time, males had a relatively constant food intake. They increased their meal size but decreased their meal number. In female rats, food intake was relatively stable for the duration of the study, despite cyclically and reciprocally recurring changes in meal number and meal size, which are synchronized with the estrous cycle. Data confirm that net food intake is a dynamic process and suggest that, in the rat, the homeostasis of food intake in response to external as well as internal stimuli is maintained via the modulation of meal number and size.

Animals↗

PubMed1996

The isolation, purification and identification of fumitremorgin B produced by Aspergillus fumigatus.

Twenty-six strains of Aspergillus fumigatus were screened for toxigenicity for fumitremorgins A and B. Twenty-three of 26 strains can produce fumitremorgin B in rice medium determined by TLC and HPLC, and no fumitremorgin A was detected. The strains of no. C4104 and no. 3656 were inoculated onto 5 kg of rice media and incubated in a modified procedure. Finally, 4.0 g of fumitremorgin B was obtained after extraction and purification by modified methods, and was confirmed by TLC, HPLC, spectral analysis together with other physicochemical analysis. This is the first report of the preparation of fumitremorgin B in China.

Aspergillus fumigatus↗

PubMed1996

The preparation and identification of fumitremorgin B-hemisuccinate-carrier proteins.

A method for the preparation and identification of fumitremorgin B-hemisuccinate-carrier protein is described. The overall yield of the fumitremorgin B-hemisuccinate (FTBS) after final purification was 78.6%. The FTBS was characterized by UV, IR, EIMS, element analysis, and 1H, 13C NMR. IR was also used to determine the formation of complete antigen complexes. The reaction route was analysized.

Immunoglobulin G↗