| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Neuroscience Program, Surgical Metabolism and Nutrition Laboratory, Department of Surgery, University Hospital, State University of New York Health Science Center, Syracuse, New York 13210; 2 Department of Metabolic Care and Gerontology, Charles University, Czech Republic; and 3 Department of Clinical Medicine, University "La Sapienza," 00185 Rome, Italy
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Because food intake is a function of meal number and meal size and because gender-related hormones are involved in feeding regulation, we explored effects of orchiectomy and testosterone replacement on the relationship between meal number and size and changes in resulting feeding patterns in adult male rats, randomized into orchiectomy and sham-operation groups. A rat eater meter measured feeding indexes for 1 wk before and 2 wk after castration and during 8 days of testosterone replacement. Orchiectomy leads to an immediate change in the meal number-to-size relationship, resulting in 1) change in pattern of feeding; 2) a significant decrease in dark-phase meal number; 3) a significant increase in dark-phase meal size, but insufficient to offset decrease in meal number, so total food intake significantly decreased during dark phase; 4) no significant change in light-phase meal number; and 5) an increase in meal size leading to an increased food intake during light phase, which offset decreased food intake in dark cycle and resulted in no net significant change in food intake after orchiectomy. Testosterone replacement acutely reversed effects of orchiectomy on meal number-to-meal size relationship, restoring feeding pattern. Data suggest that androgens immediately influence the meal number-to-meal size relationship. The speed of onset seen after orchiectomy suggests that the influence of testosterone on food intake may also occur partially via a nongenomic effect.
male Fischer rats; food intake; rat eater meter
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
GENDER-RELATED HORMONES are involved in the regulation of food intake in rats (10, 44), hamsters (40), and mice (4, 29). Orchiectomy in the adult males decreases food intake, an effect reversed by systemic administration of testosterone in physiological doses. A different effect is seen in the female: ovariectomy induces hyperphagia accompanied by increased meal size and decreased meal number (5, 43). The alterations in females appear to correlate with changing estradiol concentrations, as shown in experiments with ovariectomized rats (5) and with estradiol replacement therapy (5, 44).
Much of the detailed investigation into the gonadal control of food intake has focused on its chronic effects for two reasons. First, estrogens and androgens are steroids with well known temporal genomic activity: the effect of estrogen withdrawal on food intake in the female rat is transient, whereas the effect of androgen withdrawal in the male rat is relatively permanent (29). Second, orchiectomy significantly decreases the rate of body weight gain, whereas total food intake is reported to be only slightly decreased or not at all (14, 29, 40). In contrast, ovariectomy results in profound increase of food intake (5). These findings suggest that a slower time course of androgen effects total food intake.
Changes in microstructure of feeding, as measured by a bar pressor technique 2 wk after orchiectomy in adult male mice, showed a slightly decreased food intake with a 3-day mean reduction in meal number (MN) and a significant increase in meal size (MZ; Ref. 29). Testosterone replacement produced a dose-related fall in MZ and a corresponding rise in MN. However, feeding-related behavior differs between mice and rats (28), and a bar press procedure, a trained conditional response, could result in an exceptionally higher occurrence of small meals. Moreover, a recent report indicates that some orchiectomy-related biochemical events, which may be associated with altered MN and MZ, occur already within 2 days of orchiectomy (27) and thus 1) are not restricted to the more delayed periods of observations previously reported and 2) suggest that testosterone may influence food intake, MN, and MZ via its nongenomic activity.
Rats regulate their daily food intake by varying either the size of a meal (MZ), the interval between meals (i.e., MN), or both. As pointed out by Becker and Kissileff (3), counterbalancing controls may exist so that a change in one will produce a compensatory change in the other to preserve a relative consistency of daily food intake. In the past, we demonstrated this reciprocity of MZ and MN via a series of internal and external perturbations (for review, see Ref. 19). To function as compensatory mechanisms, it is likely that MZ and MN are independently regulated in different yet connected anatomic sites of the brain, in a way analogous to the reciprocal innervation controlling spinal reflexes. Anatomic, electrophysiological, and pathophysiological data exist that show that, in the hypothalamus, as an example, the ventromedial nucleus (VMN) and the lateral hypothalamic area (LHA) interact to influence MN and MZ. Similar anatomic, electrophysiological, and pathophysiological data for the paraventricular nucleus (PVN) in relation to other hypothalamic nuclei are currently lacking. Thus the VMN and the LHA may well represent part, among other anatomic sites, of the putative food intake-regulating areas. Superseding the dualistic theory of food intake control (1), Panksepp (26) suggested that the recurrence of short-term and long-term satiety, mediated by the LHA and the VMN, respectively, determines food intake. We and others have updated Panksepp's hypothesis by proposing that the LHA contributes to the modulation of MZ and the VMN to MN (12, 20, 21, 24, 39, 45, 46).
Because gonadal hormones influence the hypothalamus and food intake, we hypothesized that immediately after orchiectomy a change in food intake, MZ, and MN occurs. Such a change in feeding pattern may indirectly reflect the influence of testosterone's action (genomic and nongenomic) on the VMN and LHA, among other hypothalamic nuclei. Thus the aim of our study was to use orchiectomy and testosterone replacement in male Fischer rats to explore the MN-to-MZ relationship and thereby to gain insight, by inference, into the influence that testosterone may have on food intake regulation on the hypothalamus.
| |
MATERIAL AND METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Experimental Subjects
The study was approved by the Committee for the Humane Use of Animals at State University of New York Health Science Center at Syracuse; animals were cared for in accordance with the guidelines established by the National Institutes of Health. Fifteen male Fischer-344 rats (7-8 wk old; Charles River, Wilmington, MA; initial body weight 250-270 g) were housed in wire holding cages for 10 days to acclimatize them to constant study environmental conditions of a 12:12-h light-dark cycle (6:00 AM-6:00 PM), 45% relative humidity, and a room temperature of 26 ± 1°C. Rats were allowed free access to tap water and to fresh coarsely ground standard rat chow (diet #5008; Ralston Purina, St. Louis, MO; approximate macronutrient composition in %: 49 carbohydrate, 27 fat, and 24 protein). No provisions were made for dietary self-selection either before or after orchiectomy because this was not the aim of this study.Automated Computerized Rat Eater Meter and Feeding Pattern Measurements
After acclimatization, the rats were individually placed in metabolic cages equipped with the automated computerized rat eater meter (ACREM; Ref. 18). Fresh coarsely ground standard rat chow and fresh water were provided each morning at 8:00 AM, and body weight was measured every 3 days.Briefly, the ACREM consists of commercially available metabolic cages in which the supplied feeding cup situated at the end of a feeding tunnel is replaced by an electronic scale balance, and two photoelectric cells are centered above the food dish. A real-time remote computerized data collection device integrates feeding activity as measured by the electronic scale and the photocells. The ACREM characterizes feeding activity of the rat by its access to the food cup, some of which included food consumption and some of which did not. A meal was defined as a bite or series of bites with food consumption preceded and followed by at least 5 min of no food consumption, whereas a sniff was defined as access to the food cup, associated with both olfactory and vibrissal exploration of the food cup, during which no food was consumed (18).
Food intake and feeding-related indexes were measured continuously and expressed per study period [e.g., per 24 h; per 12 h during dark period (6:00 PM-6:00 AM), or per 12 h during light period (6:00 AM-6:00 PM)]. The indexes were meal number = total number of meals in each study period; meal size (g/meal) = total amount of food consumed per total meal number in each study period; and food intake (g) = amount of food consumed per study period.
Orchiectomy and Sham Operation
After the baseline feeding pattern was obtained for all rats (days
8 to
1), eight rats were
orchiectomized at day
0 under general anesthesia (ketamine
HCl 150 mg, xylazine HCl 30 mg, and acepromazine 5 mg; 0.6 ml/kg im of
the mixture). A 1-cm skin incision was made at the tip of the scrotum;
then a 5-mm incision was made into each sac at the tip of each testis,
and the cauda epididymis was pulled out, accompanied by the testis and
followed by the caput epididymis. The vas deferens and spermatic blood
vessels were ligated, severed, and the testis were removed. In another seven male rats under anesthesia a sham operation was performed in
which the testis and epididymis were only pulled out and then replaced
and the blood vessels were left intact.
The rats were returned to their ACREMs after operation. Measurement of body weight, food intake, MN, and MZ were immediately started and continuously measured for the next 2 wk (day 0-day 13). After that, there was a hiatus of 14 days, during which the rats were kept in ACREMs but only the body weight and the total food intake were measured. This was followed by another 8-day ACREM period (days 27-34) during which testosterone replacement therapy was given.
Testosterone Replacement
Testosterone (testosterone enanthate, BTG Pharmaceuticals, Inselin, NJ) was administered in eight orchiectomized rats according to the dose schedule of Gentry and Wade (10). A dose of 0.2 mg testosterone in 0.1 ml corn oil was given daily at 8:30 AM for 8 consecutive days by intramuscular injection. Sham-operated rats had daily intramuscular injections of 0.1 ml corn oil.Statistical Analysis
The feeding indexes of MN, MZ, and food intake were analyzed separately for 24 h, for light-phase, and for dark-phase feeding. All data are expressed as means ± SE. ANOVA was used to analyze the time course data within the groups. The two-tailed Student's t-test was used to compare findings between orchiectomized rats and sham-operated controls and between findings from hormone replacement in orchiectomized rats with those from sham-operated controls injected with a vehicle. A statistically significant difference was considered as a probability <0.05. Within groups, t-tests were also used to compare the pooled mean data from days8 to 1 (preoperation) with
days
3-13
(postoperation). Because the feeding pattern normalized within 3 days
during testosterone injection in orchiectomized rats, the data from the
8-day testosterone and/or vehicle treatment period were pooled from
days
30 to
34 (testosterone replacement), without
the first 3 injection days.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
MN
Before operation. As shown in Fig. 1, before operation (orchiectomy or sham operation) there was no difference between the two groups in 24-h, dark-phase, or light-phase MN.
|
After operation. Immediately after operation, 24 h MN decreased in both groups, probably secondary to the effects of anesthesia. However, the decrease in MN was significantly lower in the orchiectomy group compared with the control group. Control rats recovered from operation by day 3. From day 3 to day 13, MN did not significantly change in sham-operated controls. In orchiectomized rats it decreased significantly (P < 0.01) and was also significantly lower than in the controls (P < 0.01; Fig. 1). Immediately after operation, dark-phase MN decreased in both groups, but was significantly lower in the orchiectomy group than in the control group. In orchiectomized rats after day 3 (when the rats had recovered from operation) and until day 13, dark-phase MN decreased significantly compared with control and preoperative values (P < 0.01). Sham-operation had no effect on dark-phase mean MN, which did not change significantly compared with preoperative values (Fig. 1). Light-phase MN increased postoperatively in both groups (P < 0.05 in sham-operated group; not significantly in orchiectomized rats; Fig. 1).
MZ
Before operation. As shown in Fig. 2, mean 24-h, dark-phase, and light-phase MZ were all similar in both groups preoperatively.
|
After operation. Immediately after operation, mean 24-h MZ decreased in orchiectomized rats. After day 3 and until day 13, daily MZ increased in orchiectomized rats (P < 0.01 compared with controls and to preoperative values), but did not change in sham-operated rats (Fig. 2). Immediately after operation, daily MZ decreased in orchiectomized rats. After day 3 and until day 13 dark-phase MZ increased in orchiectomized rats (P < 0.01 compared with control and preoperation), but did not change in sham-operated rats (Fig. 2). After day 3 and until day 13 light-phase MZ increased in orchiectomized rats (P < 0.05 compared with control; P < 0.01 compared with preoperatively), but did not change in sham-operated rats (Fig. 2).
Food Intake
Before operation. Figure 3 shows that mean 24-h and mean 12-h dark- and light-phase food intake did not differ between orchiectomized rats and sham-operated controls.
|
After operation. Immediately after operation, mean 24-h food intake decreased in both groups but was significantly lower in the orchiectomy group. After day 3 and until day 13 daily food intake was slightly lower in orchiectomized rats than in sham-operated controls (P = 0.09; Fig. 3). Dark-phase food intake decreased immediately after operation in both groups and was significantly lower in the orchiectomy group.
After day 3 and until day 13 mean postoperative dark-phase food intake was significantly lower in orchiectomized compared with sham-operated rats (P < 0.01). Compared with the preoperative period, dark-phase food intake after operation was significantly lower in both orchiectomized rats (P < 0.05) and sham-operated controls (P < 0.05; Fig. 3). Immediately after operation, light-phase food intake decreased in both groups and was significantly lower in the orchiectomy group. Compared with preoperative values, after day 3 and until day 13 mean light-phase food intake was increased in both groups (P < 0.05). The light-phase food intake was significantly higher on days 6, 10, 11, and 13 in orchiectomized compared with the sham-operated rats; mean postoperative light-phase food intake comparisons had borderline significance (P = 0.054; Fig. 3).
Body Weight
Table 1 summarizes changes in mean body weights after orchiectomy, sham operation, and after testosterone replacement therapy. Body weights were the same in the orchiectomized rats (266 ± 2 g) and sham-operated controls (266 ± 2 g) at the time of operation (day 0). However, significantly lower body weight was observed in orchiectomized rats compared with the sham-operated controls as soon as day 3 after operation (P < 0.01). The average daily body weight gain between day 3 (after the rats had recovered from operation) and day 24 was significantly lower in the orchiectomized rats compared with the sham-operated controls (1.0 ± 0.2 vs. 2.1 ± 0.2 g; P < 0.01). When the ~10 g loss of weight from the operative specimen (testes, epididymis, and part of the vas deferens) is taken into account, there was a body weight difference of 31 g between the two groups at day 24.
|
Testosterone Replacement
Figure 4 summarizes the changes in mean 24-h food intake and feeding pattern that occur with testosterone replacement compared with the indexes measured preoperatively and operatively.When orchiectomized rats were treated with testosterone as shown in
Fig. 4, the 24-h mean MN was not
significantly different from the controls, but it remained lower than
preoperative values in both groups (P < 0.01; Fig. 4). No significant difference in dark-phase MN was
observed in orchiectomized rats supplemented with testosterone compared
with controls (6.8 ± 0.7 vs. 6.5 ± 0.6 meals/12 h).
The dark-phase mean MN during the replacement period was significantly
lower than preoperative values in both groups
(P < 0.01). Light-phase MN was not
different between the orchiectomized rats treated with testosterone and
the controls (5.0 ± 0.4 vs. 4.8 ± 0.5 meals), nor was it
different compared with preoperative values.
|
Mean daily MZ did not differ between orchiectomized rats treated with testosterone and sham-operated controls injected with vehicle, but it increased over preoperative values in both groups (P < 0.05; Fig. 4). Mean dark-phase MZ did not differ between orchiectomized rats treated with testosterone and sham-operated controls injected with vehicle (1.4 ± 0.1 vs. 1.5 ± 0.2 meals), nor was it different from preoperative values in both groups. Mean light-phase MZ did not differ between orchiectomized rats treated with testosterone and sham-operated controls injected with vehicle, but it was significantly increased over preoperative values in both groups (1.3 ± 0.1 and 1.5 ± 0.1 meals; P < 0.01).
Daily food intake in orchiectomized rats treated with testosterone was not significantly different compared with controls treated with vehicle only and to preoperative values (Fig. 4). After testosterone treatment, dark-phase food intake was not significantly different from sham-operated controls injected with vehicle (9.1 ± 0.5 vs. 9.4 ± 0.4 g). In both groups, food intake in the testosterone-replacement period was significantly lower than the preoperative values (P < 0.05). The light-phase food intake was similar in testosterone-replaced rats and in controls (6.2 ± 0.3 and 6.8 ± 0.5 g).
In orchiectomized rats, body weight increased with testosterone replacement therapy to 272 ± 5 g at day 33 (Table 1), which was still significantly lower than the body weight in sham-operated rats (314 ± 4 g; P < 0.01). Body weight gain between days 27 and 33 slightly increased in the orchiectomized rats with testosterone replacement therapy but did not differ significantly between groups (1.2 ± 0.3 vs. 1.7 ± 0.3 g).
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
In young adult male Fischer-344 rats, the ACREM was used to measure the immediate changes in daily, as well as the dark- and the light-phase MN, MZ, and total food intake before and after orchiectomy and then after testosterone replacement. Our findings confirmed and extended previous observations that the orchiectomized male rat significantly decreases its rate of body weight gain with slight or no decrease in daily food intake and that testosterone administration reverses the orchiectomy effect on body weight gain (10, 14, 29, 40). Our study extends information concerning the microstructural changes that occur acutely in the immediate postorchiectomy period. After orchiectomy and testosterone replacement, the immediate change in the MN-to-MZ relationship that occurred is described in RESULTS.
The modulatory effects of orchiectomy on the meal patterns of number and size are similar to those reported after total liver denervation (32) or olfactory bulbectomy (17), when compensatory changes of MN and MZ resulted in no net effect on daily food intake. Thus the present evidence supports the widely recognized concept that MN and MZ are tightly coupled to maintain the homeostasis of food intake, and, by inference, it suggests the existence of a close functional link between the hypothalamic areas influencing MN and MZ. Data have been generated suggesting that the changing levels of the neurotransmitters dopamine and serotonin in the LHA and in the VMN, among other events in other hypothalamic nuclei, such as the PVN, play a role in influencing hunger and in influencing satiety (12, 25, 39). Changing dopamine levels in the LHA correlate with changes in the size of the meal (20, 45), whereas changes in dopamine levels in the VMN related to the intermeal interval, i.e., MN (21, 46).
The role of the VMN as a target site for testosterone is well
documented, although its relationship in influencing the microstructure of food intake still needs to be completely detailed. When implants of
testosterone propionate (TP) are used, 5-
-dihydroteststerone (DHT)
propionate and 17
-estradiol, in the VMN and anterior
hypothalamus-preoptic area in castrated male rats, it was shown that TP
may act directly in the hypothalamus to influence food intake in male
rats (23). These data suggest that aromatization of testosterone to
estrogens is related to the central effects of TP on food intake,
because estradiol treatment tended to be more effective than TP in
reducing food intake. In contrast, treatment with DHT propionate, a
nonaromatizable androgen, failed to have any effect on food intake even
at a very high dose of 20 mg/day (28). Furthermore, hypothalamic
implants of estradiol benzoate in male rats reduced food intake,
whereas ovarian transplants in castrated male rats suppressed weight
gain compared with intact male rats; after removal of the ovarian
grafts, body weight increased once more (2).
The VMN of the male rat contains neurons with receptors for
testosterone, DHT, and estradiol (38), neurons that accumulate testosterone and estradiol. Testosterone acts genomically as an androgen on specific neural androgenic receptors, whereas neurons within the brain are able to metabolize circulating testosterone into
neurally active metabolites. Testosterone is converted via aromatase to
17-estradiol through the activity of a specific androgen binding
cytochrome P-450 enzyme and to DHT by
5--reductase (7). These gonadal steroid hormones may affect
ingestive behavior via an influence on neurotransmitters in several
different ways: 1) nongenomic
effects on pre- or postsynaptic membranes alter permeability to
neurotransmitters or their precursors or the functioning of
neurotransmitter receptors; 2)
genomically, by altering the synthesis of proteins that may participate
in pre- or postsynaptic events after axonal or dendritic transport.
Consistent evidence indirectly supports the possible nongenomic effects of testosterone on the VMN in modulating feeding patterns. The VMN neurons contain different subgroups of neurons, projecting to the central gray, with specific sensitivity to metabolites of testosterone (42). Mean threshold of excitation decreases after orchiectomy, but reverses with either TP or DHT. This increased excitability of the VMN neurons after orchiectomy could possibly explain the early satiety and hence lower food intake and body weight. Supporting this inference are data showing that castration reduces (36) and testosterone replacement restores VMN concentrations of neuropeptide Y (NPY) (37), a well known orexigenic neuropeptide, whose mechanism of action is based on the modulation of neuronal excitability (8). Furthermore, most of the factors influencing food intake, including interleukin-1 (30) and leptin (41), share with NPY the same mechanism of action. This indicates that modulation of neuronal excitability might represent the final pathway common to different factors in the control of food intake (15). In the ovariectomized female rat, the reverse occurs: delayed development of satiety and hence increased food intake and body weight gain. This gender difference in the biological response to castration might be explained by the anatomic (16) and functional (35) differences existing between male and female VMN.
The genomic effects of gonadal steroids on food intake are yet to be demonstrated, but they likely occur. Dopaminergic neurons play a critical role in multiple brain function, including eating activity. Tuberoinfundibular dopamine activity, a pathway involved in the regulation of prolactin, increases 2 wk after orchiectomy and declines in castrated male and female rats after 2 wk of testosterone or estradiol replacement, respectively (11). Furthermore, in the male rat, dopamine turnover increases in the median eminence 1-2 wk after orchiectomy and decreases after testosterone replacement (11). The delayed occurrence of changes in dopamine activity suggests the involvement of a genomic mechanism, and recently it has been shown that the efficacy of dopaminergic neurotransmission is regulated by a phosphoprotein DARPP-32 (9).
The effects of testosterone and gonadal steroids on LHA activity in controlling food intake are considerably less clear. However, a recent report showed that the anorectic effects of dehydroepiandrosterone in Zucker rats are mediated by changes in serotonin and dopamine levels within the LHA (31).
The catechol estrogens are unique. Because of the steroid structure
they act similar to estrogens, while, via the catechol structure, they
act similar to and compete with catecholamines. Cathechol estrogens are
potent inhibitors of tyrosine hydroxylase, the rate-limiting enzyme in
dopamine synthesis, and of
catechol-O-methyl transferase, an
enzyme involved in the inactivation of norepinephrine and dopamine.
They compete for membrane dopamine binding sites, which results in a
net increase in dopamine levels. They also block the accumulation of
dopamine and norepinephrine in the rat brain synaptosomes (13) and
directly inhibit -adrenergic or dopamine receptors (22). The VMN (2)
and the PVN (6) have also been implicated as neural sites mediating the
effects of estrogen on feeding. The catechol estrogens appear to be the
biochemical link between estrogens and catecholamines in the central
nervous system and probably modulate the circadian rhythm in feeding
via effects on the neurotransmitters.
Perspectives
On the basis of the sum of our data and the cited studies from the literature, we reason that the immediate effects of testosterone on food intake that we observe in the male rat occur probably via testosterone's nongenomic activity, likely brought about by testosterone's metabolism to estradiol. We postulate that some of the estradiol is metabolized in the hypothalamus to catechol estrogen, which has dopaminergic-like activity. The evidence in favor of this postulate is 1) testosterone can be metabolized into estradiol in various tissues including hypothalamus and adipose tissue; 2) the levels of aromatase are significantly higher in males than in females and in the anterior hypothalmus and the VMN (34), in the nucleus of stria terminalis, the medial preoptic nucleus, and medial and cortical amygdala (33); 3) progesterone reduces the weight-reducing effect of a high testosterone dose similar to its reversal of the weight-reducing effect of estradiol; 4) high doses of DHT (nonaromatizable androgen) do not suppress weight gain in male rats; and finally, 5) testosterone reduces body weight by reducing adipose tissue mass.| |
ACKNOWLEDGEMENTS |
|---|
The work presented in this paper was supported in part by National Institute of Diabetes and Digestive and Kidney Diseases Grant DK-43796 and the American Institute for Cancer Research Grant 85A95. Dr. Blaha is supported by the National Institutes of Health Short Term Scientists Exchange Program of the National Cancer Institute.
| |
FOOTNOTES |
|---|
Present address of J.-K. Chai: 304 Hospital, Beijing, P.R. China.
Address for reprint requests and other correspondence: M. M. Meguid, Dept. of Surgery, Univ. Hospital, 750 East Adams St., Syracuse, NY 13210.
Received 10 January 1997; accepted in final form 4 February 1999.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Anand, B. K.,
and
J. R. Brobeck.
Hypothalamic control of food intake in rats and cats.
Yale J. Biol. Med.
24:
123-140,
1951[Medline].
2.
Beatty, W. W.,
D. A. O'Brien,
and
T. R. Vilberg.
Suppression of feeding by intrahypothalamic implants of estradiol in male and female rats.
Bull. Psychonom. Soc.
3:
273-274,
1974.
3.
Becker, E. E.,
and
H. R. Kissileff.
Inhibitory controls of feeding by the ventromedial hypothalamus.
Am. J. Physiol.
226:
383,
1974.
4.
Blank, J. L.,
A. I. Korytko,
D. A. Freeman,
and
T. P. Ruf.
Role of gonadal steroids and inhibitory photoperiod in regulating body weight and food intake in deer mice.
Proc. Soc. Exp. Biol. Med.
206:
396-403,
1994[Abstract].
5.
Blaustein, J. D.,
and
G. N. Wade.
Ovarian influences on the meal patterns of female rats.
Physiol. Behav.
17:
201-208,
1976[Medline].
6.
Butera, P. C.,
and
R. J. Biekirch.
Central implants of diluted estradiol: independent effects on ingestive and reproductive behaviors of ovariectomized rats.
Brain Res.
491:
266-273,
1989[Medline].
7.
Celotti, F.,
R. C. Melcangi,
and
L. Martini.
The 5 alpha reductase in the brain: molecular aspects and relation to brain function.
Front. Neuroendocrinol.
13:
163-215,
1992[Medline].
8.
Erickson, J. C.,
K. E. Clegg,
and
R. D. Palmiter.
Sensitivity to leptin and susceptibility to seizures of mice lacking neuropeptide Y.
Nature
381:
415-418,
1996[Medline].
9.
Fienberg, A. A.,
N. Hiroi,
P. G. Mermelstein,
W. Song,
G. L. Snyder,
A. Nishi,
A. Cheramy,
J. P. O'Callaghan,
D. B. Miller,
D. G. Cole,
R. Corbett,
C. N. Haile,
D. C. Cooper,
S. P. Onn,
A. A. Grace,
C. C. Ouimet,
F. J. White,
S. E. Hyman,
D. J. Surmeier,
J. Girault,
E. J. Nestler,
and
P. Greengard.
DARPP-32: regulator of the efficacy of dopaminergic neurotransmission.
Science
281:
838-842,
1998
10.
Gentry, R. T.,
and
G. N. Wade.
Androgenic control of food intake and body weight in male rats.
J. Comp. Physiol. Psychol.
90:
18-25,
1976[Medline].
11.
Gunnet, J. W.,
K. J. Lookingland,
and
K. E. Moore.
Comparison of the effects of castration and steroid replacement on incerto-hypothalamic dopaminergic neurons in male and female rats.
Neuroendocrinology
44:
269-275,
1986[Medline].
12.
Hoebel, B. G.,
L. Hernandez,
D. H. Schwartz,
G. P. Mark,
and
G. A. Hunter.
Microdialysis studies of brain norepinephrine, serotonin and dopamine release during ingestive behavior: theoretical and clinical implications.
Ann. NY Acad. Sci.
575:
171-191,
1989.
13.
Inaba, M.,
and
K. Kamata.
Effect of estradiol 17 beta and other steroids on noradrenaline and dopamine binding to synaptic membrane fragments of the rat brain.
J. Steroid Biochem.
11:
1491-1497,
1979[Medline].
14.
Kakolewski, J. W.,
C. C. Verne,
and
E. S. Valenstein.
Sex differences in body-weight change following gonadectomy of rats.
Psychol. Rep.
22:
547-554,
1968[Medline].
15.
Laviano, A.,
F. Rossi Fanelli,
and
M. M. Meguid.
The brain's normal function (Abstract).
Science
280:
503,
1998.
16.
Matsumoto, A.,
and
Y. Arai.
Male-female difference in synaptic organization of the ventromedial nucleus of the hypothalamus in the rat.
Neuroendocrinology
42:
232-236,
1986[Medline].
17.
Meguid, M. M.,
J. R. Gleason,
and
Z.-J. Yang.
Olfactory bulbectomy in rats modulates feeding pattern but not total food intake.
Physiol. Behav.
54:
471-475,
1993[Medline].
18.
Meguid, M. M.,
Y. Kawashima,
A. C. L. Campos,
P. Gelling,
T. W. Hill,
T.-Y. Chen,
D. C. Hitch,
and
W. J. Mueller.
Automated computerized rat eater meter: description and application.
Physiol. Behav.
48:
759-763,
1990[Medline].
19.
Meguid, M. M.,
Z.-J. Yang,
and
J. R. Gleason.
The gut-brain brain-gut axis in anorexia: towards an understanding of food intake regulation.
Nutrition
12:
S57-S62,
1996[Medline].
20.
Meguid, M. M.,
Z.-J. Yang,
and
M. Koseki.
Eating induced rise in LHA-dopamine correlates with meal size in normal and bulbectomized rats.
Brain Res. Bull.
36:
487-490,
1995[Medline].
21.
Meguid, M. M.,
Z.-J. Yang,
and
A. Laviano.
Meal size and number: relationship to dopamine levels in the ventromedial hypothalamic nucleus.
Am. J. Physiol.
272 (Regulatory Integrative Comp. Physiol. 41):
R1925-R1930,
1997
22.
Moore, R. Y.,
and
V. B. Eichler.
Loss of circadian adrenal corticosterone rhythm following suprachiasmatic lesion in the rat.
Brain Res.
42:
201-206,
1972[Medline].
23.
Nunez, A. A.,
L. I. Siegel,
and
G. N. Wade.
Central effects of testosterone on food intake in male rats.
Physiol. Behav.
24:
469-472,
1980[Medline].
24.
Oomura, Y.,
H. Ooyama,
T. Yamamoto,
and
F. Naka.
Reciprocal relationship of the lateral and ventromedial hypothalamus in the regulation of food intake.
Physiol. Behav.
2:
97-115,
1967.
25.
Orosco, M.,
and
S. Nicolaidis.
Spontaneous feeding-related monoaminergic changes in the rostromedial hypothalamus revealed by microdialysis.
Physiol. Behav.
52:
1015-1019,
1992[Medline].
26.
Panksepp, J.
Hypothalamic regulation of energy balance and feeding behavior.
Federation Proc.
33:
1150-1165,
1974[Medline].
27.
Park, S. K.,
D. A. Strouse,
and
M. Selmanoff.
Prolactin- and testosterone-induced inhibition of LH secretion after orchidectomy: role of catecholaminergic neurones terminating in the diagonal band of Broca, medial preoptic nucleus and median eminence.
J. Endocrinol.
148:
291-301,
1996[Abstract].
28.
Petersen, S.
The temporal pattern of feeding over the oestrus cycle of the mouse.
Anim. Behav.
24:
939-955,
1976[Medline].
29.
Petersen, S.
Effects of testosterone upon feeding in male mice.
Anim. Behav.
26:
945-952,
1978[Medline].
30.
Plata-Salaman, C. R.,
and
J. M. Ffrench-Mullen.
Interleukin-1 beta depresses calcium currents in CA1 hippocampal neurons at pathophysiological concentrations.
Brain Res. Bull.
29:
221-223,
1992[Medline].
31.
Porter, J. R.,
J. M. Abadie,
B. E. Wright,
E. S. Browne,
and
F. Svec.
The effect of discontinuing dehydroepiandrosterone supplementation on Zucker rat food intake and hypothalamic neurotransmitters.
Int. J. Obes. Relat. Metab. Disord.
19:
480-488,
1995[Medline].
32.
Ratto, C.,
J. R. Gleason,
Z.-J. Yang,
R. Bellantone,
F. Crucitti,
and
M. M. Meguid.
Change in meal size, number and duration after neural isolation of liver and with TPN.
Physiol. Behav.
50:
607-612,
1991[Medline].
33.
Roselli, C. E.,
W. E. Ellinwood,
and
J. A. Resko.
Regulation of brain aromatase activity in rats.
Endocrinology
114:
192-200,
1985[Abstract].
34.
Roselli, C. E.,
L. E. Horton,
and
J. A. Resko.
Regulation of brain aromatase activity in rats.
Endocrinology
117:
2471-2477,
1984[Abstract].
35.
Sahu, A.,
W. R. Crowley,
P. S. Kalra,
and
S. P. Kalra.
A selective sexually dimorphic response in the median eminence neuropeptide Y.
Brain Res.
573:
235-242,
1992[Medline].
36.
Sahu, A.,
S. P. Kalra,
W. R. Crowley,
and
P. S. Kalra.
Testosterone raises neuropeptide-Y concentrations in selected hypothalamic sites and in vitro release from the medial basal hypothalamus of castrated male rats.
Endocrinology
124:
410-414,
1989[Abstract].
37.
Sahu, A.,
P. S. Kalra,
W. R. Crowley,
and
S. P. Kalra.
Functional heterogeneity in neuropeptide-Y-producing cells in the rat brain as revealed by testosterone action.
Endocrinology
127:
2307-2312,
1990[Abstract].
38.
Sar, M.,
and
W. E. Stumpf.
Distribution of androgen target cells in rat forebrain and pituitary after [3H]-dihydrotestosterone administration.
J. Steroid Biochem.
8:
1131-1135,
1997.
39.
Schwartz, D. H.,
S. McClane,
L. Hernandez,
and
B. G. Hoebel.
Feeding increases extracellular serotonin in the lateral hypothalamus of the rat as measured by microdialysis.
Brain Res.
479:
349-354,
1989[Medline].
40.
Slusser, W. N.,
and
G. N. Wade.
Testicular effects on food intake, body weight, and body composition in male hamsters.
Physiol. Behav.
27:
637-640,
1981[Medline].
41.
Spanswick, D.,
M. A. Smith,
V. E. Groppi,
S. D. Logan,
and
M. L. Ashford.
Leptin inhibits hypothalamic neurons by activation of ATP-sensitive potassium channels.
Nature
390:
521-525,
1997[Medline].
42.
Suga, S.,
and
Y. Sakuma.
Dihydrotestosterone-sensitive neurons in the male rat ventromedial hypothalamus.
Brain Res. Bull.
33:
205-210,
1994[Medline].
43.
Varma, M.,
R. Evangelista,
M. M. Meguid,
L. Han,
B. Li,
J.-K. Chai,
and
Z.-J. Yang.
Estrogen effects on circadian and estrous cycle in food intake and feeding patterns.
Surg. Forum
83:
524-526,
1997.
44.
Wade, G. N.
Some effects of ovarian hormones on food intake and body weight in female rats.
J. Comp. Physiol. Psychol.
88:
183-195,
1975[Medline].
45.
Yang, Z.-J.,
M. Koseki,
M. M. Meguid,
and
A. Laviano.
Eating-related increase of dopamine concentration in the LHA with oronasal stimulation.
Am. J. Physiol.
270 (Regulatory Integrative Comp. Physiol. 39):
R315-R318,
1996
46.
Yang, Z.-J.,
M. M. Meguid,
and
A. Oler.
Eating-associated VMN-dopamine levels of rats: comparison of oral and intragastric feeding.
Neuroreport
8:
1543-1547,
1997[Medline].
This article has been cited by other articles:
|
|
 |
|
  T. Notomi, Y. Okazaki, N. Okimoto, Y. Tanaka, T. Nakamura, and M. Suzuki Effects of tower climbing exercise on bone mass, strength, and turnover in orchidectomized growing rats J Appl Physiol, September 1, 2002; 93(3): 1152 - 1158. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
