Biomedical subjects

L L Bellinger

Publications and source records attributed to L L Bellinger.

At least 37 records · Page 2Linked to original sources

PubMed1994

HPLC-purified bovine satietin suppresses food intake and weight without causing conditioned taste aversion.

Satietin (SAT) is a putative satiety agent found in a variety of species including man and the rat. In the present study, satietin was extracted from bovine plasma (b-SAT) and further high-pressure liquid chromatography (HPLC)-purified. Rats were given chronic third ventricle cannulas and patency was verified. In experiment 1, rats were divided into three groups and ICV infused with artificial cerebrospinal fluid (a-CSF) or b-SAT: group 1, a-CSF (n = 11); group 2, 20 micrograms/rat, b-SAT (n = 11); and group 3, 40 micrograms/rat, b-SAT (n = 9). Infusions were repeated thrice three days apart. Compared to a-CSF, the high b-SAT dose suppressed food intake for 24-h after each successive infusion. The low dose significantly decreased food intake only after the first infusion. Water intake was suppressed only after the first injection of the high dose. Body weight was decreased after the first and second infusions of both doses and following the third infusion of the high dose. In experiment 2, rats were trained to drink fluid for 1 h/day while food was ad lib. On day 1, both groups received no infusions and were given tap water. On day 2, the groups were ICV infused with a-CSF, but group 1 (n = 12) was given banana-flavored fluid (BFF) and group 2 (n = 12) almond-flavored fluid (AFF). On day 3, group 1 was again a-CSF-infused but given AFF, whereas group 2 received 40 micrograms/rat b-SAT and was given BFF.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1994

Hormone and somatic changes in rats pair-fed to growth retarded dorsomedial hypothalamic nuclei-lesioned rats.

Rats with dorsomedial hypothalamic nuclei lesions (DMNL) are hypophagic and have reduced linear and ponderal growth, but have normal body composition and anabolic hormone concentrations. Previous studies have shown rats pair-fed to levels consumed (70-80% of ad lib) by DMNL rats, using a meal-feeding paradigm, have abnormal body composition and hormone concentrations. Whether the noted changes were due to restriction per se or method of food presentation was uncertain. In the present study, one group of sham-operated rats was pair fed (SHPF) by a computer-operated system that presented 45 mg food pellets in the exact amount and pattern as their DMNL yoked partner; another sham-operated group was ad lib fed (SHAD). At the end of Experiment 1 (11 days) and Experiment 2 (3 weeks) blood was collected for hormone and metabolite analyses; body compositions were also determined. Unlike an earlier report, the DMNL and SHPF groups had normal percentage body fat. Percentage carcass protein was similar in all groups at 11 days, but slightly elevated in DMNL rats at 3 weeks. Also, in contrast to an earlier study, plasma-free fatty acid levels were comparable in DMNL and SHPF rats. Plasma insulin was normal in the DMNL and SHPF rats at 11 days, but was lowered (p < 0.05) in the SHPF group at 3 weeks. Plasma thyroxine was reduced (p < 0.01) in the SHPF group at 11 days but returned to normal by 3 weeks. Thyroxine and triiodothyronine levels were normal in the DMNL groups. Plasma corticosterone levels were similar in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Ingestive patterns of liver-denervated rats presented with several diets.

The liver by way of afferent nerves is suggested to be a controller of food intake. In experiment 1, male rats were given a 15% fructose solution during the first 4 h of the dark phase, while chow was available the rest of the time, for 10 days, before total liver denervation (TLD) or sham operation. Postsurgery ingestion patterns (15-min measurements for 4 h) of fructose were similar in the two groups. However, chow intake in the TLD group was slightly attenuated the first 2 days after surgery. In experiment 2, rats were given chow in cups and vegetable oil in bottles for 8 days before TLD or sham operation. After surgery, hourly ingestion of chow and oil did not differ between the groups; however, there was a trend for the TLD group to take more oil in the dark phase on the first-day diet exposure. In experiment 3, rats were fed a high-protein diet for 21 days before TLD or sham operation. With the use of a computer-operated system, postsurgery meal size, meal duration, and frequency patterns were found to be comparable between the groups. In experiment 4, rats were given a diet of sweetened condensed milk mixed with water (3:1 vol/vol) and vitamins for 14 days before hepatic vagal branch transection (HVBX) or sham operation. After surgery the first-day milk intake of both groups was similar up to 3.5 h and then depressed at 4 and 24 h in the HVBX rats, but was again comparable over the next 13 days; body weights were similar throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

PubMed1993

Hypophagic rats with dorsomedial hypothalamic lesions produce lighter and smaller pups with a lower survival rate at weaning than offspring of sham-operated controls.

Weanling and mature rats with dorsomedial hypothalamic nucleus lesions (DMNL rats) show reduced ponderal and linear growth and hypophagia and hypodipsia in the presence of normal body composition and anabolic hormone levels. The present study was conducted to assess their reproductive/parenting capacity and some offspring parameters. Four groups were used: DMNL mothers and fathers, DMNL mothers and control (SCON) fathers, SCON mothers and DMNL fathers, and SCON mothers and SCON fathers. The constituent rats of each group were bred to yield between 14 and 22 litters. The smallest litter size, litter weight, mean pup weight, percent of live-born and percent of weaned pups and greatest percentage of still-born pups were recorded when both parents were DMNL rats. The latter parents also cannibalized the majority of litters. The above parameters improved when only one parent was a DMNL rat, but this was still significantly below the offspring of SCON x SCON parents. The DMN is not part of the classical hypophysiotropic area (HTA), but earlier findings indicate hyperprolactinemia in DMNL rats. Therefore, the lesion-induced hypophagia during gestation and the postpartum neuroendocrine profile of the DMNL mothers may be the cause of the observed litter deficiencies and poor survival.

Animals↗

PubMed1993

Validation study of a total body electrical conductive (TOBEC) instrument that measures fat-free body mass.

Validation of the model SA-2's (EM-SCAN, Inc.) ability to measure fat-free body mass (FFM) and indirectly predict body fat mass using total body electrical conductivity (TOBEC) methodology was investigated. To simulate changes in FFM (6.8 to 27.2 g) and fat mass (5 to 20 g), saline and oil, respectively, were injected into multiple sites of male Sprague-Dawley rats in separate trials. Two identical experiments were conducted; only the body weights differed. In Experiment 1 the rats' starting body weight averaged 171.8 +/- 3.4 g, while it averaged 214.0 +/- 2.8 g in Experiment 2. In Experiments 1 and 2, model SA-2 was used, and theoretical changes in FFM had correlations of r = 0.88 and r = 0.82, respectively. There was a tendency of the machine to consistently overpredict FFM as greater amounts of saline were injected. In Experiment 1, when oil was injected, FFM remained extremely stable, whereas in Experiment 2, it consistently overpredicted the amount of fat added in these heavier rats. Because the overpredictions in both the cases were consistent, an adjustment to the prediction equation can possibly correct these problems. Until this is done, caution must be used in interpreting data gather from the model SA-2.

Adipose Tissue↗

PubMed1993

Liver denervation, 5-HT3 receptor antagonist, and intake of imbalanced amino acid diet.

The serotonin3 receptor antagonist ICS 205-930 (ICS) may act peripherally to attenuate the anorectic response of rats given an imbalanced amino acid (IMB) diet. Rats were divided into four groups: SHAM+saline (sal); SHAM+ICS; total liver denervation (TLD) + sal; and TLD+ICS. Rats were then given a purified basal diet for 16 days. Next, the groups were injected with sal or 9 mg/kg BW of ICS at 0800 h and at 0900 h (lights out) an isoleucine IMB diet was presented. By 12 h postinjection, the food intake (FI) of TLD and SHAM rats receiving ICS was similarly higher (p < 0.02) than sal-injected counterparts whose FI was also similar; BW followed FI. By day 3, the SHAM groups had similar low FI, whereas the FI of the TLD groups was increasing. The above study was repeated with similar results. Liver innervation is not required for ICS attenuation of IMB diet-induced hypophagia. Also, while sal-injected TLD rats show a normal attenuation of consumption of the IMB diet on the first day of exposure, they subsequently consume more of the IMB diet than SHAM rats. The reason for this difference in TLD rats is not clear but may be related to metabolism of the IMB diet or possibly learning.

Amino Acids↗

PubMed1993

The lateral hypothalamic area revisited: neuroanatomy, body weight regulation, neuroendocrinology and metabolism.

This article reviews findings that have accumulated since the original description of the syndrome that follows destruction of the lateral hypothalamic area (LHA). These data comprise the areas of neuroanatomy, body weight regulation, neuroendocrinology, neurochemistry, and intermediary metabolism. Neurons in the LHA are the largest in the hypothalamus, and are topographically well organized. The LHA belongs to the parasympathetic area of the hypothalamus, and connects with all major parts of the brain and the major hypothalamic nuclei. Rats with LHA lesions regulate their body weight set point in a primary manner and not because of destruction of a "feeding center". The lower body weight is not due to finickiness. In the early stages of the syndrome, catabolism and running activity are enhanced, and so is the activity of the sympathetic nervous system (SNS) as shown by increased norepinephrine excretion that normalizes one mo later. The LHA plays a role in the feedback control of body weight regulation different from ventromedial (VMN) and dorsomedial (DMN). Tissue preparations from the LHA promote glucose utilization and insulin release. Although it does not belong to the classical hypothysiotropic area of the hypothalamus, the LHA does affect neuroendocrine secretions. No plasma data on growth hormone are available following electrolytic lesions LHA but electrical stimulation fails to elicit GH secretion. Nevertheless, antiserum raised against the 1-37 fragment of human GHRF stains numerous perikarya in the dorsolateral LHA. The plasma circadian corticosterone rhythm is disrupted in LHA lesioned rats, but this is unlikely due to destruction of intrinsic oscillators. Stimulation studies show a profound role of the LHA in glucose metabolism (glycolysis, glycogenesis, gluconeogenesis), this mechanism being cholinergic. Its role in lipolysis appears not to be critical. In general, stimulation of the VMN elicits opposite effects. Lesion studies in rats show altered in vitro glucose carbon incorporation into several tissue fractions both a few days, and one mo after lesion production. Several of these changes may be due to the reduced food intake, others appear to be due to a "true" lesion effect.

Animals↗

PubMed1992

Metabolic and neuroendocrine indices one month after lateral hypothalamic area lesions.

Mature male rats received bilateral electrolytic lateral hypothalamic area lesions (LHAL) or were sham-operated fed ad lib (CON-ADLIB) or sham-operated pair-fed/gained (CON-PF) to LHAL rats. One month later all rats were sacrificed. Rats with LHAL were hypophagic and had reduced body carcass fat, testes, livers, epididymal fat pads (PADS), diaphragms (DIA), and body weight compared to CON-ADLIB. In the liver, LHAL rats incorporated more C14-U-glucose carbon (GLUCINC) into lipid and glycogen than both CON groups, but GLUCINC was similar among CON groups. In PADS, LHAL rats oxidized more glucose carbon (GLUCOX) than CON-ADLIB but less than CON-PF/PG. The latter showed greater GLUCOX than CON-ADLIB. In DIA, LHAL and CON-PF/PG showed reduced GLUCINC into glycogen vs. CON-ADLIB. Plasma glucose was similar among groups, but insulin was lower in LHAL and CON-ADLIB than in CON-PF/PG. Rats with LHAL had lower plasma T3 concentrations than CON-ADLIB, but similar T3 levels compared to CON-PF/PG. Several of the metabolic changes in LHAL rats could be due to hypophagia; however, four out of nine metabolic indices, glucose carbon incorporation into liver lipid and glycogen and epididymal fat pad lipid and oxidation, were significantly different from CON-PF/PG, i.e., they were independent of food intake. Possibly then, they are due to a lesion effect other than on feeding mechanisms. Some aspects of metabolism that were previously found to be altered 48 h after LHAL were recovered, whereas others apparently were not.

Adipose Tissue↗

PubMed1991

Brown (BAT) and white (WAT) adipose tissue in high-fat junk food (HFJF) and chow-fed rats with dorsomedial hypothalamic lesions (DMNL rats).

Male weanling rats received dorsomedial hypothalamic nucleus lesions (DMNL) or sham operations and were fed for 173 postoperative days a high-fat diet and given a 32% sucrose solution as drinking fluid. This was supplemented with chocolate chip cookies, potato chips and marshmallows. Other DMNL and sham-operated controls were fed lab chow instead of the above high-fat junk food diet (HFJF) and given tap water instead of 32% sucrose solution. All animals were killed on postoperative day 174. Caloric intake per 100 g body weight was similar in all groups; however, the HFJF fed control and DMNL rats had significantly elevated carcass fat. Since HFJF-DMNL rats were not nearly as obese as the HFJF control animals, it appears that the DMNL offered some protection against the HFJF-diet-produced obesity. When their smaller body size is considered. DMN lesions had no effect on brown adipose tissue (BAT) mass in chow-fed or HFJF fed rats, whereas BAT size was significantly enlarged in HFJF-fed control animals. This suggests but does not prove that HFJF-fed controls, but not DMNL rats, may be using dietary-induced thermogenesis (DIT) to attenuate their obesity. We hypothesize that the HFJF-fed DMNL may not be enhancing DIT as reflected in normal BAT size, because they had not attained a degree of fatness to activate this system, or the DMN lesions impaired its activation. Both HFJF-fed groups showed reduced linear growth compared to their counterparts. The reason for stunting is uncertain, but may be related to their low plasma insulin concentrations.

Adipose Tissue↗

PubMed1991

HPLC-purified human satietin does not produce conditioned taste aversion in rats.

Human satietin is thought to be an endogenous glycoprotein that can suppress food intake and body weight. However, it was also found to be aversive when rats infused intracerebroventricularly (ICV) with human satietin were subjected to a two-bottle taste aversion test. More recently, the human satietin previously thought homogenous was separated by HPLC into two Peaks, denoted as A and B. In the present study, male Sprague-Dawley rats were fitted with chronic third ventricle cannulas and presented with fluid for 1 h/day, while food was given ad lib. After training, the rats were ICV infused with either artificial cerebrospinal fluid, Peak A or Peak B of human satietin. Peak B significantly reduced short-term and 24-h food intake, whereas their fluid intake was nonsignificantly attenuated. Peak A had no affect on either food or fluid intake on the day it was administered. When the rats were given the two-bottle taste aversion test neither compound was found to be aversive. These data suggest that Peak B may contain satietin(s) which could be a candidate for an endogenous satiety agent.

Animals↗

PubMed1991

Liver denervation does not alter the circadian rhythm of bile acid synthesis in rats.

In both rats and humans there is a distinct circadian rhythm of bile acid synthesis that is independent of feedback regulation. To determine whether the circadian rhythm is directly mediated via hepatic nerves, bile acid synthesis was studied in selectively liver-denervated male Sprague-Dawley rats in a bile fistula model. Complete denervation was confirmed by histofluorescent staining for neural elements in frozen sections of livers. There was no significant difference in mean bile acid synthesis, amplitude of the circadian rhythm, or time of peak synthesis between the denervated rats and nondenervated controls. In one denervated rat studied four times at weekly intervals, there was no shift in acrophase, indicating that the rhythm had not become free running. We conclude that signals arriving via hepatic nerves neither directly cause nor entrain the circadian rhythm of bile acid synthesis in rats.

Animals↗

PubMed1990

Somatic, endocrine and metabolic changes in controls pair-fed for six weeks to rats with dorsomedial hypothalamic nucleus lesions (DMNL rats).

One group of weanling male Sprague-Dawley rats received lesions in the dorsomedial hypothalamic nuclei (DMNL rats), whereas two additional groups of rats were sham-operated (CON). One of these CON groups was allowed to feed ad lib (CON-ADLIB) while the other CON group was pair-fed for 6 weeks to the DMNL rats (CON-PF). Despite eating the same amount of food as DMNL rats. CON-PF animals had consistently lower body weights and also utilized food energy more poorly than DMNL rats. The CON-PF group also had smaller kidneys and less percent liver protein but more epididymal fat pad percent protein than DMNL rats. Whereas plasma glucose concentrations were comparable among the three groups, insulin levels were significantly higher, and free fatty acid levels lower in CON-PF than in DMNL rats. The CON-PF group incorporated less glucose-U-C14 carbon into liver glycogen but more of the tracer into liver lipid than the DMNL group. Glucose carbon was also incorporated more avidly into epididymal fat pad lipid by CON-PF than by DMNL rats. The data not only confirm previous findings in DMNL rats but in addition show that the neurologically intact rats fed the same amount of food that is eaten spontaneously by DMNL rats show somatic and metabolic alterations that suggest that they cannot cope with this low amount of substrate. The normalcy of the DMNL rats, compared to ad lib-fed sham-operated controls, in all metabolic parameters suggests that the low food intake is indeed "normal" for this preparation and may be the reflection of an "organismic" set point.

Animals↗

PubMed1990

The effect of portal infusions of epinephrine on ingestion, plasma glucose and insulin in dogs.

Preabsorptive satiety has been hypothesized to occur as the result of food activating oral and gastrointestinal receptors that cause the release of catecholamines in the liver. The catecholamines were then proposed to hyperpolarize hepatic glucoreceptors and produce satiety. In the present study the hepatic portal vein was chronically cannulated in six mongrel dogs. Upon recovery the dogs were infused, over three minutes, with either saline or epinephrine (0.83 and 1.5 micrograms/kg b. wt.). Infusions ended 10 minutes prior to the animals' daily one-hour feeding period. The epinephrine infusions resulted in physiological increases in plasma glucose and insulin, but did not inhibit food consumption. The animals were next prefed 20% of their normal daily food intake 30 minutes prior to infusion of epinephrine at the above noted doses. Again plasma glucose and insulin increased, but food consumption was not affected. These data show that epinephrine infusions which produce physiological changes in plasma glucose and insulin do not alter feeding behavior of mongrel dogs. These findings are in agreement with previous data that question the physiological importance of the preabsorptive catecholamine satiety hypothesis.

Animals↗

PubMed1990

Metabolic-endocrine correlates of the lateral hypothalamic syndrome: the first 48 hours.

Mature (224 g) male Sprague-Dawley rats received bilateral electrolytic (1 mA for 8 sec) lesions in the lateral hypothalamic area (LHAL) or sham operations (CON). One group of CON was allowed to eat ad lib (CON-ADLIB), a second CON group was pair-fed to the LHAL rats (CON-PF). Tap water was available ad lib. Two days after the operation/sham operation all rats were killed by decapitation. Body weight, body weight change, food intake, carcass fat, liver weight, epididymal fat pad weight, in vitro incorporation of U-C14-glucose into liver total lipid, glycogen and CO2 (oxidation) (DPM, DPM/mg protein) as well as oxidation in fat pad tissue, plasma glucose and insulin were significantly reduced in LHAL and CON-PF rats compared with CON-ADLIB. Glucose carbon incorporation into epididymal fat pad lipid and glycogen were normal in LHAL and CON-PF. Liver protein and plasma free fatty acids (FFA) were both higher in LHAL and CON-PF than in CON-ADLIB groups. Thus, many of the somatic and metabolic changes that appear in the first few days after lesion production are simply due to hypophagia. However, CON-PF rats also exhibited some significant differences from the LHAL group, i.e., their plasma glucose and incorporation of glucose carbon into liver glycogen (DPM) were significantly lower than in LHAL rats; alternatively, plasma FFA levels were higher in CON-PF than in LHAL rats. Also, liver weight/100 g body weight was lower and fat pad weight/100 g body weight was higher in CON-PF than in LHAL rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1990

The effects of semi- and HPLC-purified human satietin and alpha-1-glycoprotein on ingestion and body weight.

Satietin is thought to be an endogenous glycoprotein that can suppress food intake (FI) and body weight (b.wt.). In Experiment 1, rats were ICV infused with either a-CSF or with 50 micrograms/rat of human satietin. FI was suppressed (p less than 0.05) for 2 days after infusion, whereas b.wt. was attenuated (p less than 0.05) for 14 days. In Experiment 2, the previously thought homogenous human satietin was further purified by HPLC and this yielded two peaks (A and B). Rats were ICV infused with either a-CSF or 50 micrograms/rat of Peak A, Peak B or the semipurified parent human satietin (sph-SAT) from which the peaks were derived. All three treatments suppressed (p less than 0.05) FI on day 1 after infusion and on day 2 in the groups that received Peak A and sph-SAT. Body weight was attenuated (p less than 0.01) in all the experimental groups on day 1 and for 2 and 10 days, respectively, in the Peak A and sph-SAT-treated groups. Immunostaining revealed Peak A contained both albumin and alpha-1-glycoprotein (A1G), whereas Peak B contained neither. In the last experiment rats were ICV infused with either a-CSF or 50 micrograms/rat of A1G or A1G that was put through the sph-SAT extraction procedure. FI was suppressed (p less than 0.01) and b.wt. attenuated in both experimental groups only on the first day postinfusion. These data suggest that some, but possibly not all, of the previously found biological activity attributed to sph-SAT might be due to contaminants of the preparation.

Albumins↗

PubMed1990

Effect of liver denervation on compensatory changes in food intake, body composition and hepatic enzyme induction after food restriction in rats.

The mechanisms involved in the recovery of body fat and liver metabolism after food restriction and refeeding are not understood. This study's aim was to determine the need for hepatic neural input for the compensatory changes in food intake, body composition and hepatic lipogenic enzymes seen upon realimentation after energy restriction. Rats underwent total surgical hepatic denervation or had sham operations. One group of sham-operated and denervated rats was fed a semipurified diet ad libitum; a second group was restricted to 40% ad libitum levels for 7 d, then given free access to food during a 2-d refeeding period. Body fat content and body fat recovery rate from below "set point" were not altered by hepatic denervation. These observations do not rule out liver involvement because blood-borne factors communicating energy status information to the central nervous system could be released from the liver. The activities of hepatic enzymes--glucose-6-phosphate dehydrogenase, malic enzyme and citrate cleavage enzyme--were stimulated at least twofold by restriction and refeeding when compared to ad libitum feeding. Hepatic denervation had no effect on basal enzyme levels in ad libitum-fed animals or on elevated enzyme activity induced by refeeding after food restriction. This study clearly demonstrates that hepatic innervation is not essential for energy balance and body composition regulation. The induction of lipogenic enzymes by food restriction and refeeding does not depend on central nervous system input to the liver.

ATP Citrate (pro-S)-Lyase↗

PubMed1989

Growth hormone secretion and ultradian rhythms in growth-retarded rats with dorsomedial hypothalamic lesions.

Rats with lesions of the dorsomedial nucleus of the hypothalamus (DMN-L) are hypophagic and have reduced linear growth and body weight, but normal body composition. Male Sprague-Dawley rats (170-190 g) housed individually under a 12:12 L:D schedule with lights out at 1430 hr received jugular cannulas, and on return to precannulation body weight (4.2 +/- 0.6 days), they received bilateral electrolytic DMN-L or sham-operations (SHAM). Rats with DMN-L (n = 8) were hypophagic postsurgery and weight less (p less than 0.05) than SHAM at six days postlesion surgery. The difference in body weight between the two groups continued to expand over the next four weeks. Six days postsurgery, the rats were bled (RBC's returned in 10% BSA-saline) every 15 minutes between 0600-1215 hr and growth hormone (GH) subsequently assayed. The total GH secretion, as computed from the area under each rat's ultradian pattern, was similar in both groups (DMN-L versus SHAM, 2952.2 +/- 346.5 versus 2950.4 +/- 337.5). Using the PULSAR computer program, the baseline secretion (12.2 +/- 4.0 versus 11.8 +/- 2.7 ng/ml), total number of peaks (2.4 +/- 0.4 versus 2.4 +/- 0.2), and interpeak interval (2.8 +/- 0.5 versus 2.7 +/- 0.4, hr) were not significantly different between the DMN-L and SHAM rats, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

The effect of portal and jugular infused glucose, mannitol and saline on food intake in dogs.

Hepatic glucoreceptors have been hypothesized to have an important role in determining normal hunger and satiety. In the present study 23 dogs were fitted with chronic hepatic portal and jugular vein cannulas. The dogs were fed for 1 hr/day. On infusion days (total of 318 infusions) the animals were infused into the portal or jugular veins with a 30% glucose solution (2.4 or 3.6 g/kg, b.wt.), 0.9% NaCl as a volume control or 30% mannitol as an osmotic control and then fed 10 minutes later. The data showed that the dog's food consumption was similar after they received glucose or the appropriate control infusion regardless of the infusion site. Some dogs had blood samples taken for glucose and insulin determinations prior to infusion, at the middle and end of infusion, just prior to food presentation and at the end of the feeding period. Saline and mannitol infusions did not alter plasma glucose or insulin concentrations; whereas there were marked increases in plasma glucose (6-8 x) and insulin (18-19 x) following glucose infusions. Postinfusion glucose values indicated approximately 72% of the infused dose glucose (approximately 43 g) had left the plasma prior to food presentation. Despite the large increases in plasma glucose and insulin, as well as glucose storage and/or oxidation, the dogs consumed amounts of food similar to that eaten after control infusions. Similarly, prefeeding the dogs 20% of their average daily intake prior to infusion did not alter the animals subsequent intake. These data are in agreement with earlier work from our laboratory and question the role of the hypothesized hepatic glucose satiety receptors.

Animals↗