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Biomedical subjects

T Sakata

Publications and source records attributed to T Sakata.

At least 19 recordsLinked to original sources
PubMed1996

Ornithine decarboxylase activity in rat intestinal mucosa and liver is stimulated by central administration of 2-deoxy-D-glucose but not of 2,5-anhydro-D-mannitol.

It has been shown that 2-deoxy-D-glucose (2-DG) inhibits glucose utilization and elicits feeding through the lateral hypothalamus. In contrast, 2,5-anhydro-D-mannitol (2,5-AM), blocking glycogenolysis and/or gluconeogenesis, elicits feeding through the ventromedial hypothalamus. The aim of the present study was to determine whether ornithine decarboxylase (ODC) activity in the rat small intestine is stimulated by infusion into the third ventricle of 2-DG or of 2,5-AM. Under anesthesia, a cannula was implanted into the third ventricle one week before the experiment. Each rat was infused with 6, 12, and 24 mumol 2-DG or 2,5-AM into the third ventricle without disturbing the behavior. Ingestive behavior was observed for one h after the infusion. ODC activity in the intestinal mucosa and the liver was measured 2 h after the infusion. Additionally, ODC activity was measured in vagotomized rats. Both test solutions elicit feeding at 24 mumol/rat. Infusion of 2-DG into the cerebroventricle significantly increased ODC activity in the duodenal and jejunal mucosa and the liver. In contrast to 2-DG, infusion of 2,5-AM did not increase ODC activity in the intestinal mucosa or liver. Truncal vagotomy attenuated the increase of ODC activity in the intestinal mucosa and liver induced by 2-DG. The present study showed that 2-DG, but not 2,5-AM, increased ODC activity in the peripheral organs, indicating that glucose-metabolism at specific sites of the central nervous system, including the lateral hypothalamus, is important for stimulatory signals to ODC activity. It is also indicated that the stimulatory signals from the central nervous system are mediated, at least in part, via the efferent vagal nerve.

Animals↗
PubMed1996

Clinical significance of activated protein C resistance as a potential marker for hypercoagulable state.

The activated protein C (APC)-resistance test is a simple and reliable method for detecting reduced sensitivity to the anticoagulant action of this protein. We investigated the sensitivity to APC in 180 Japanese controls and in 96 Japanese patients with venous and arterial thrombosis (28 with deep vein thrombosis; 13 with pulmonary thromboembolism; 41 with cerebral infarction; and 14 with coronary artery disease). All of the patient groups showed significantly reduced sensitivity to APC, reflected by the lower normalized APC-sensitivity ratio (n-APC-SR), as compared with healthy control. The APC-sensitivity ratio was negatively correlated with plasma activated factor VII levels. These results suggest that the low n-APC-SR is related to venous or arterial thrombotic disease. The APC resistance may serve as a potential marker for assessing the hypercoagulable state.

Adult↗
PubMed1996

Clearance of phenytoin and valproic acid is affected by a small body weight reduction in an epileptic obese patient: a case study.

The interaction between clearance of phenytoin, valproic acid, phenobarbital and carbamazepine, and changes in body weight was determined in a 19-year-old obese woman with epilepsy (body weight 93 kg, BMI 36.3 kg/m2). The patient, who was given daily oral doses of 100 mg phenobarbital, 350 mg phenytoin, 800 mg valproic acid and 800 mg carbamazepine over 5 months was hospitalized for obesity treatment. The daily dosage of each drug was held constant during treatment of the obesity. Blood samples were taken five times. Weight reduction was 7 kg (7.5%) over 46 days. Estimation of the pharmacokinetic parameters in each drug was performed by Higuchi's Bayesian program, PEDA Pearson's correlation coefficient (r) between clearance and body weight was calculated for each drug. High positive correlations were found between clearance and body weight for phenytoin (r = 0.800) and valproic acid (r = 0.785), but not for phenobarbital (r = -0.227) and carbamazepine (r = 0.152). Clearance of phenytoin and valproic acid may be potentially affected by small changes in body weight.

Adult↗
PubMed1996

Transplantation of lean fetal hypothalamus restores hypothalamic function in Zucker obese rats.

Rats with lesions to the ventromedial hypothalamus (VMH) manifest obesity, hyperphagia, and hyperinsulinemia, and fetal VMH transplantation into the third cerebroventricle of VMH-lesioned rats reduces the development of obesity caused by the lesion. The aim of this study was to determine whether the hyperphagia, hyperlipidemia, and hyperinsulinemia of obsese Zucker rats could be corrected by the transplantation of lean fetal Zucker hypothalamic tissue into the third cerebral ventricle of Zucker obese rats. After the fetal hypothalamic transplant (obese-HY), the rate of weight gain was significantly diminished compared with the unoperated Zucker obese rats and the obese rats that received the transplantation of a similar amount of frontal cortical tissue from the same fetus (obese-FC). Food intake was significantly lower, and plasma triacylglycerol and insulin concentrations were also significantly reduced in the obese-HY rats compared with the obese and obese-FC rats. The weight of the adrenal glands, the plasma adrenocorticotropic hormone concentration, the liver weight, and the liver lipid content in obese-HY were significantly less than those observed in the obese and obese-FC animals. There were no significant differences between the obese and the obese-FC animals or between unoperated Zucker lean rats and lean rats transplanted with lean fetal hypothalamus in all the parameters we determined in this study. Neovascularization and normal cellular morphology of the transplanted fetal hypothalamic tissue suggest that the transplanted neural and glial cells were viable and physiologically functional. In conclusion, this study offers evidence suggesting that the hypothalamic-pituitary-adrenal function is defective in Zucker obese rats, resulting in excessive weight gain, hyperphagia, hyperlipidemia, and hyperinsulinemia. The hypothalamic dysfunction in the Zucker obese rats is corrected by the transplantation of lean fetal hypothalamus.

Adrenal Glands↗
PubMed1996

Factor VII hyperactivity and endothelial cell damage are found in elderly hypertensives only when concomitant with microalbuminuria.

We studied the relationship among albuminuria, factor VII (FVII) hyperactivity, and endothelial cell damage in 6 elderly hypertensive subjects. The plasma levels of activated FVII (FVIIa), FVII coagulant activity, FVII antigen (FVIIag), von Willebrand factor (vWF), and thrombomodulin were measured to assess FVII hyperactivity and endothelial cell damage, and urinary albumin excretion rate (UAE) was calculated using 12-hour nighttime (7 pm to 7 am) urine collection (mean for 2 consecutive nights). We performed 24-hour ambulatory blood pressure monitoring in all 61 hypertensive patients and classified them into a white-coat hypertension group (n=12) and a sustained hypertension group (n=49). For the levels of FVII, vWF, and thrombomodulin, there were no differences between the white-coat hypertension group and normotensive control subjects (n=25). In the sustained hypertensive group, only the microalbuminuric subgroup (UAE, 15 to 300 microgram/min: n=30) showed significant elevation compared with the normotensive group for the level of FVIIa (mean [95% confidence interval]: 4.0 [3.6 to 4.4] versus 3.0 [2.6 to 3.3] ng/mL, P<.001), the FVIIa/FVIIag ratio (an indicator of activation of FVII zymogen to FVIIa) (1.33 [1.19 to 1.50] versus 1.04 [0.92 to 1.19], P<.01), the level of vWF (188 [165 to 214] % versus 144 [129 to 160] %, P<.01), and thrombomodulin (11.7 [10.3 to 13.3] versus 9.3 [8.5 to 10.3] ng/mL, P<.01). In contrast, none of these levels in the normoalbuminuric hypertensive group (UAE <15 microgram/min, n=19) differed from that in the normotensive control group. These results suggest that among elderly hypertensives, only those with microalbuminuria show enhancement of FVII activation and endothelial cell damage, while patients with white-coat hypertension and normoalbuminuric hypertensives do not show these accompanying abnormalities. Thus, increased levels of FVII activity and markers of endothelial cell damage might account for the higher risk of cardiovascular events in essential hypertension with microalbuminuria.

Aged↗
PubMed1996

Plasminogen activator inhibitor-1 in nonobese subjects with non-insulin-dependent diabetes mellitus.

Elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been shown to be a risk factor for the development of vascular complications in obese and hyperinsulinemic non-insulin-dependent diabetes (NIDDM) patients. To clarify whether PAI-1 also plays an essential role in the development of such complications in NIDDM patients without obesity or hyperinsulinemia, PAI-1 was analyzed in relation to blood pressure, fasting plasma levels of glucose (FPG), hemoglobin A1C (HbA1c), immunoreactive insulin (F-IRI), C-peptide (CPR), total cholesterol (TC), triglyceride (TGL), and HDL-cholesterol (HDL-C) in 77 NIDDM patients and 10 healthy control subjects. The NIDDM patients were not obese (body mass index [BMI]:<26 kg/m2) or hyperinsulinemic, and BMI in the controls was between 19 and 24 kg/m2. In addition, parameters of insulin secretion reserve, including sigmaIRI, insulinogenic index, and CPR at 5 min after glucagon loading, were evaluated simultaneously. Plasma levels of PAI-1 were higher in the NIDDM group (9.3+/-0.9 ng/ml) than in the controls (4.3+/-0.7 ng/ml;P<0.01). Levels of FPG and HbA1c were also elevated in the NIDDM group (P<0.05 for each), but F-IRI did not differ between the two groups. However, multiple regression analysis revealed no significant correlation in the NIDDM between PAI-1 and F-IRI or the parameters of insulin secretion reserve. Regardless of the presence or absence of vascular complications, PAI-1 did not vary significantly in the NIDDM. These findings suggest that the effects of PAI-1 on the development of diabetic complications in NIDDM patients may not proceed in the same way in those with versus those without obesity or hyperinsulinemia, because no correlation was found between PAI-1 and insulin secretion reserve, while plasma levels of PAI-1 were higher in the NIDDM group than in the controls.

Adult↗
PubMed1996

[A patient with Goodpasture's syndrome revealed a poor prognosis regardless of receiving intensive therapy from an early stage after onset].

Goodpasture's syndrome has been reported as a disease that has a favorable prognosis when the patient receives intensive immunosuppressive drug-therapy from an early stage after onset. The present report describes a 50-year-old woman, who exhibited progressive renal failure accompanied by pulmonary hemorrhage, and an increase in serum level of antiglomerular basement membrane (GBM) antibody. Initial histological examination of a renal specimen indicated a severe fibrocellular crescentic glomerulonephritis with a linear deposition of Ig-G and C3 along the glomerular capillary wall. The patient was thus diagnosed as having Goodpasture's syndrome. Therapy with pulse treatment of steroid (corticosteroid hormone), immunosuppressive agents, or plasma-exchange for the removal of anti-GBM antibody was adopted a week after the clinical onset. However, histological amelioration of the glomeruli did not occur with this treatment in the second biopsy, while glomerular damage advanced progressively. In contrast to other patients with Goodpasture's syndrome, our case revealed an unfavorable outcome regardless of receiving intensive therapy from an early period after onset, which suggests that more intensive therapy of another approach to this patient may have been necessary.

Anti-Glomerular Basement Membrane Disease↗
PubMed1996

[Bronchobiliary fistula].

A 57-year-old woman with congenital syphilis had a productive cough, fever, cholecystolithiasis, and paralytic ileus. She had a 30-year history of recurrent bronchitis accompanied by yellowish serous sputum. A chest radiograph showed bilateral infiltrates resulting from aspiration pneumonia, and a reduction in volume of the right middle and right lower lobes. After recovering from paralytic ileus, she still had fever and biliptysis. Bronchoscopy revealed bile filling the right basal bronchi. Emergency laparotomy and throacotomy revealed a gall stone, splenomegaly, marked atrophy of the right lobe of the liver, and adhesion between the right pleura and the diaphragm. A T-tube cholangiogram showed that the right hepatic duct communicated with the right basal bronchus. Despite ligation of the right hepatic duct, biliptysis continued. The patient died due to rapidly progressing hepatorenal failure. Syphilis gummosa due to congenital syphilis was suspected as a cause of the bronchobiliary fistula, but was not confirmed pathologically. The surgical specimen showed only nonspecific fibrosis with calcification. Bronchobiliary fistula is rare in Japan; we know of only 6 other reported cases.

Biliary Fistula↗
PubMed1996

[Saprophytic pleuritis with Candida parapsilosis].

A 73-year-old man was admitted to our hospital with pneumonia in the right S6 induced by Streptococcus milleri and with left pleural thickening. He had histories of diabetes mellitus for 30 years and pulmonary tuberculosis 35 years ago. The pneumonia resolved completely after administration of ceftazidime and clindamycin for 10 days, but the pleural thickening remained and computed tomography revealed that it was an encapsulated effusion without calcification. An aspirate was turbid yellow with a high concentration of lipids, and consisted of dominant crystals and scattered cells, 80% of which were yeasts and 20% of which were macrophages phagocytizing them. Only Candida parapsilosis developed in culture. The same silent pleural shadow was identified on chest X-ray films obtained over the previous 7 years. The persistent pleuritis was diagnosed as saprophytic infection with C. parapsilosis.

Aged↗
PubMed1995

Pharmacological evidence for the persistent activation of ATP-sensitive K+ channels in early phase of reperfusion and its protective role against myocardial stunning.

BACKGROUND: The activation of cardiac ATP-sensitive potassium channels is reported to protect myocardium during ischemia. However, the behavior and role of this channel during reperfusion remain uncertain. METHODS AND RESULTS: Guinea pig right ventricular walls were studied by use of microelectrodes and a force transducer. Each preparation was perfused via the coronary artery at a constant flow rate and was stimulated at 3 Hz. In the first protocol, the preparation was subjected to 10 minutes of no-flow ischemia, which was followed by 60 minutes of reperfusion. Introduction of ischemia shortened the action potential duration (APD) to 58.7 +/- 3.1% of the preischemic values, in association with a decrease in the resting membrane potential (by 12 +/- 0.8 mV) and action potential amplitude (by 34.6 +/- 1.8 mV). On reperfusion, although the APD was restored, it remained shortened for up to approximately 30 minutes of reperfusion. In the presence of glibenclamide (10 mumol/L), the shortening of the APD during ischemia was significantly attenuated and the restoration of APD after reperfusion was significantly facilitated. When glibenclamide was applied from the onset of reperfusion, the persistent APD shortening was significantly suppressed. The developed tension decreased during ischemia and recovered after 60 minutes of reperfusion (up to 92.0 +/- 6.4% of preischemic values) in the untreated preparations. The application of glibenclamide that was started before ischemia or from the onset of reperfusion significantly suppressed the recovery of contractility (P < .05 versus untreated preparations). In the second series of experiments, 20 minutes of no-flow ischemia and 60 minutes of reperfusion were applied. This protocol produced a sustained contractile dysfunction after reperfusion (to 34.0 +/- 3.2% of preischemic values). In the presence of cromakalim (2 mumol/L), the APD shortening was enhanced during both ischemia and the early reperfusion period. Cromakalim significantly improved the contractile recovery (to 79.3 +/- 4.1% of preischemic values, P < .05 versus untreated preparations). The application of cromakalim that was started from the onset of reperfusion also improved the contractile recovery during this phase and this effect was associated with enhanced APD shortening. However, the cromakalim-treated preparations demonstrated a higher incidence of ventricular fibrillation during reperfusion. CONCLUSIONS: Cardiac ATP-sensitive potassium channels are activated by ischemia, and a fraction of these channels remains activated during the early reperfusion phase. The resulting shortening of the APD prevents the heart from developing myocardial stunning.

Action Potentials↗
PubMed1995

Induction of TCR-gamma delta+ cells from thymocytes stimulated by a fetal liver-derived hepatocyte clone.

We have previously reported that a fetal liver-derived hepatocyte clone, FHC-4D2, can support hematopoiesis in vitro. Here, we show that fetal thymocytes (FT) or adult thymocytes (AT) proliferate on the monolayer of FHC-4D2 cells in the presence of rIL-2. Fresh thymocytes contained few TCR-gamma delta+ cells (< 4% for FT and < 1% for AT); significant numbers of TCR-gamma delta+ cells were detected (2-11% for FT and 15-33% for AT) after the coculture with FHC-4D2 and rIL-2. Although FT-derived TCR-gamma delta+ cells predominantly used the V gamma 5 chain, the major population in AT-derived TCR-gamma delta+ cells used V gamma 1, V gamma 4, or V gamma 7 chains. Both FT- and AT-derived TCR-gamma delta+ cells killed FcR-bearing target cells when incubated with anti-TCR-gamma delta Ab. Half of FT-derived TCR-gamma delta+ cells were CD4-CD8 alpha+8 beta-; the rest were CD4-CD8 alpha-8 beta-. AT-derived TCR-gamma delta+ cells expressed neither CD4 nor CD8 molecules. Separation of thymocytes from FHC-4D2 cells with a membrane filter reduced the proliferative response by two- to threefold. Taken together, these results demonstrate that a fetal hepatocyte clone supports thymocytes to develop preferentially into TCR-gamma delta+ cells in cooperation with rIL-2 through cell-cell contact, that the repertoire and the phenotype of induced TCR-gamma delta+ cells are determined by the age of the mice, and that hepatocytes might thus play an active role in T lymphopoiesis in the fetal liver.

Age Factors↗
PubMed1995

alpha-amylase inhibitor increases plasma 3-hydroxybutyric acid in food-restricted rats.

The effect on energy metabolism of delayed absorption of starch by inhibition of alpha-amylase was examined by considering levels of plasma glucose and 3-hydroxybutyric acid (3-OHBA) in rats. Addition of alpha-amylase inhibitor (alpha AI) to a high starch diet delayed the plasma glucose response after feeding: peak plasma glucose levels in the control group occurred 15 min after feeding, whereas in the alpha AI group this peak did not occur until 30 min after. The total plasma glucose response was not different between the two groups. Plasma 3-OHBA levels 1 day after food restriction increased approximately five-fold in both groups. After 3 days of food restriction, the alpha AI group maintained the same level of plasma 3-OHBA as after 1 day of food restriction, while the control group showed significantly decreased levels of 3-OHBA. After 3 days of food restriction, plasma insulin levels were significantly decreased in the alpha AI group compared with the corresponding levels of the control group and with levels before the restriction. There was no significant difference in body weight between the two groups. These findings suggest that delayed hyperglycemia due to delayed absorption of starch following alpha AI loading may attenuate insulin secretion, leading to altered metabolism of 3-OHBA during the delayed response to energy deficit.

3-Hydroxybutyric Acid↗
PubMed1995

Silent cortical strokes associated with atrial fibrillation.

To clarify whether silent cortical strokes (SCS) could be a predictor of symptomatic stroke in patients with atrial fibrillation (AF), 72 patients with AF (50 with chronic AF, 22 with paroxysmal AF) were studied. Patients with mitral stenosis, history of myocardial infarction, or dilated cardiomyopathy were excluded from this study. Using cranial magnetic resonance imaging (MRI), the patients were divided into those with SCS (23 patients, Group 1) and those without SCS (49 patients, Group 2). The incidence of symptomatic stroke was then compared between the two groups. Three patients (13%) in Group 1 developed symptomatic brain infarction; this is statistically significant (p < 0.05), compared with the patients in Group 2, none of whom experienced symptomatic stroke. We suggest that SCS is a predictor of symptomatic cerebral infarct in patients with AF. Therefore, it is thought to be important to diagnose SCS using cranial MRI or computed tomography and to keep patients with SCS under close surveillance.

Aged↗
PubMed1995

Histamine receptor and its regulation of energy metabolism.

In a series of studies on brain functions of histamine, probes to manipulate activities of histaminergic neuronal systems were applied to assess histaminergic function in non-obese normal, and lean and obese Zucker rats. Food intake was suppressed by both activation of H1-receptors and inhibition of H3-receptors in the ventromedial hypothalamic nucleus (VMH) and the paraventricular nucleus, each of which is a satiety center. Feeding circadian rhythm was decreased in its amplitude through histaminergic modulation in the hypothalamus. Histamine neurons in the mesencephalic trigeminal nucleus (Me5) were involved in regulation of masticatory functions, particularly eating speed, while histamine-containing neurons in the VMH controlled intake volume of meals. Energy deficiency in the brain enhanced satiation through histaminergic activation of VMH neurons, which in turn produced glycogenolysis in the hypothalamus to maintain homoestatic control of glucose supply. A very-low-calorie conventional Japanese diet, which is a fiber rich and low energy food source, enhanced satiation by increased mastication and because of the low energy supply of the diet. Hypothalamic histamine neurons were activated by high ambient temperature and also by interleukin-1 beta, an endogenous pyrogen, to maintain homeostatic thermoregulation. Behavioral and metabolic abnormalities of Zucker obese rats were mediated by a deficit in hypothalamic neuronal histamine, and the Zucker rat was evaluated as an animal model of histamine deficiency. Transplantation of the lean fetal hypothalamus into the third cerebroventricle of host obese Zuckers attenuated the abnormalities.

Animals↗
PubMed1995

A very-low-calorie conventional Japanese diet: its implications for prevention of obesity.

A very-low-calorie conventional Japanese diet of 370 kcal/day has been shown to be useful for weight reduction and its long-term maintenance. Sources of the diet were mainly from chicken fillet, egg white, fish white-meat, mushroom, seaweed and low- or non-calorie fiber-rich vegetable, and contained 4.4g fat, 38.1g protein, 45.2g carbohydrate and essential minerals and vitamins. However, metabolic and neural implications of a commercial very-low-calorie liquid formula diet have rarely been investigated from the view point of food intake and appetite regulation. Animal studies have demonstrated the rationale for efficacy of the very-low calorie conventional Japanese diet as follows: (1) Increased hypothalamic histamine suppressed food intake through H1-receptors in the ventromedial hypothalamus (VMH) and paraventricular nucleus, the satiety centers. (2) Low energy intake enhanced satiety and decreased food intake through histaminergic activation of VMH neurons. (3) Mastication activated afferent signal transmission from proprioceptors in the oral cavity to the mesencephalic trigeminal nucleus(Me5). Histaminergic systems in the hypothalamus were activated by mastication and low energy supply, which was accompanied by satiation through the action of histamine in the VMH. Usefulness of the very-low-calorie conventional Japanese diet derives from utilization of conventional Japanese food stuffs as a fiber rich, low energy food source, and from enhancement of satiation by increased mastication required of the diet. The properties of the diet seemed to effect a closed positive feedback loop between histaminergic activation in hypothalamic satiety centers and behavioral changes to enhance satiation and cause feeding suppression.

Diet, Reducing↗
PubMed1995

Effects of auricular acupuncture stimulation on nonobese, healthy volunteer subjects.

Effects of auricular acupuncture stimulation on nonobese healthy volunteers were investigated. Subjects (n = 35) averaged 34.5 years old, and BMI was 25.3 kg/m2. Small (0.15 x 2.0 mm) auricular needles were applied intracutaneously into the bilateral cavum conchae that was identified by having less than 100 k omega resistance. Body weight was measured four times a day and charted by the subjects themselves. Results showed that, in the period 11-2, in which only body weight was measured, without auricular acupuncture stimulations, 57.1% of the subjects reduced their body weight. This indicates that charting body weight themselves might be useful to maintain their weight. In the auricular acupuncture treated period, 19 (70.4%) out of 27 decreased (p < 0.01), 5 (18.5%) was increased, and 3 (11.1%) had no change in body weight. In conclusion, the results suggest that success in maintaining weight reduction can be attributed to graphic illustration of one's weight pattern. Bilateral auricular acupuncture stimulation can also reduce body weight of healthy non-obese subjects. This is consistent with the suggestion that it might be effective in the treatment of obese patients.

Acupuncture Points↗
PubMed1995

Apolipoprotein A-IV: a circulating satiety signal produced by the small intestine.

How fat feeding, especially lipoproteins and apolipoproteins, may affect food intake is unclear. Apolipoprotein A-IV (apo A-IV) is a protein associated with chylomicrons, and its synthesis by the small intestine is markedly stimulated following ingestion of fat. We explored the anorectic effect of chylous lymph on feeding behavior. Intestinal lymph samples collected during lipid infusion intraduodenally when administered intravenously markedly suppressed food intake in fasting rats. To determine if the suppressor was lipid or apo A-IV, fasting rats were infused intravenously with a 2% Intralipid emulsion, but it did not suppress food intake. These data suggest that the factor in chylous lymph that suppresses food intake is probably apo A-IV. To test this, apo A-IV in chylous lymph was removed by immunoprecipitation, and the chylous lymph with apo A-IV removed lost its anorectic effect. Next, we infused purified apo A-IV intravenously in fasted rat, and it inhibited food intake in a dose-dependent manner. We therefore conclude that increased apo A-IV in chylous lymph is a factor involved in anorexia after fat feeding. Infusion of 0.5 microgram of apo A-IV into the third ventricle failed to suppress food intake. Higher doses (1 microgram or higher) of apo A-IV infused into the third ventricle inhibited food intake in a dose-dependent manner. To further test the hypothesis that apo A-IV is an important factor controlling food intake, we administered goat anti-rat apo A-IV serum into the third ventricle of rats that were allowed food and water ad libitum. In all rats tested, this treatment resulted in enhanced food intake. In conclusion, we propose that apo A-IV may act centrally to control food intake.

Animals↗