[Saliva secretion and oral health in a hospitalized geriatric population in Israel].

Saliva secretion decreases with age, although not regarded as caused solely by age. The decrease is associated among others, with diseases and medications. The aim of the study was to assess saliva secretion, dentition and oral pathologies in a hospitalized geriatric population in a genera hospital. The secretion was measured by 2 methods: saliva collection at rest and sugar cube test. 125 patients agreed to participate, with an average age of 75. They had an average of 6 diagnoses, and took 6 medications. They had 6 teeth in average, with 52% edentulous. Salivary excretion was found to be 15% low according to the saliva secretion and According to the sugar cube test, 20% suffer from xerostomia. However, no statistically significant correlations were found to age, medications, diagnoses, or number of teeth. The study population was hospitalised for short term in a general hospital, and quickly returned to the community. Therefore, we can conclude that salivary excretion is low in the geriatric population in the community, especially among those who suffer from illnesses, who need short terms hospitalization. The health care personnel should be aware of this situation and recommend saliva substitutes and stimulants.

Estrous cycle irregularities in overfed rats.

Hypothalamic and genetic obesities in rodents are usually associated with reproductive impairments, but the underlying etiology of the latter is not clear because of concomitant metabolic abnormalities in these animal models. In the present study metabolically intact rats were used and obesity was developed by offering the rats a cafeteria-type diet. Purina chow-fed animals were used as control. Cafeteria feeding was associated with hyperphagia and an increased brown adipose tissue (BAT) thermogenesis, in association with long estrous cycles (p less than 0.01). The latter was accounted for by a long diestrous phase (p less than 0.02). Replacement of the cafeteria diet with purina rat chow corrected the estrous cycle irregularities, as caloric consumption and body weight were reduced. We propose, as a working hypothesis, that reproductive functions are finely tuned with body temperature, and that an excess feeding-induced BAT thermogenesis may underlie the disruption in estrous cycle observed during overfeeding.

Meal associated changes in brown fat thermogenesis and glycogen.

Data indicate a close association between a decrease in feeding-induced brown adipose tissue (BAT) thermogenesis and an increase in food consumption. The present study examines the hypothesis that feeding-induced BAT thermogenesis, or feeding-induced changes in BAT glycogen, a mobile form of energy store and a correlate of BAT thermogenesis, may modulate feeding behavior. We report that propranolol, which completely abolished meal-induced BAT thermogenesis, did not evoke intake of a larger meal. Though BAT glycogen concentration is a sensitive measure of the state of feeding, on a meal to meal basis it does not correlate with hunger and satiety. Hence the hypothesis is not supported by the current data. We also report that meal-induced BAT hypertrophy and glycogen deposition can be dissociated from meal-induced BAT thermogenesis.

Thermogenic capacity and brown fat in rats exercise-trained by running.

Brown adipose tissue, a major effector of nonshivering thermogenesis (NST) in mammals, is activated by the sympathetic neurotransmitter norepinephrine. Prolonged increases in norepinephrine levels, whether elicited by cold exposure or exogenous application of catecholamines, lead to increased NST and increased thermogenic capacity of brown fat. Exercise training is also accompanied by enhanced sympathetic activity. The possibility exists that this enhancement may alter brown fat function. The present study was designed to assess the effect of a running exercise regimen on whole animal NST and the in vivo response of brown fat. Rats were trained by running on a treadmill (an average of 17 m/min, 0 degrees incline, for 90 min/d) for a period of at least 6 weeks. Whole animal NST capacity was assessed by monitoring oxygen consumption in response to infusion of norepinephrine. As a measure of the contribution of brown fat to whole body NST, the mass and norepinephrine-stimulated blood flow (microsphere technique) to the tissue were measured. None of these variables differed between the exercised (n = 10) and sedentary (n = 10) groups. That is, there were no significant differences between the two groups with respect to resting oxygen consumption, norepinephrine-induced oxygen consumption, brown fat mass, and brown fat blood flow--whether expressed per gram of tissue or as total tissue blood flow (ie, tissue mass X blood flow per gram). Further study is needed to explain the differential responses of brown fat to the increased sympathetic activity occurring during exercise v that occurring during cold exposure.

Cold-induced increase in brown fat thyroxine 5'-monodeiodinase is attenuated in Zucker obese rat.

In this study we examined the possibility that the reduced brown adipose tissue (BAT) thermogenesis in the Zucker obese rat may result from a limited capacity for enzymic conversion of thyroxine (T4) to triiodothyronine (T3) in BAT. A total of 34 lean and obese rats, approximately 4 mo old were divided into three treatment groups: group 1 (5 lean and 6 obese) was fed Purina rat chow for 21 days, and group 2 (5 lean and 6 obese) was fed a cafeteria diet for 21 days, and group 3 (6 lean and 6 obese) was fed Purina rat chow and maintained in the cold (8 +/- 1 degrees C) for 7 days. The lean and obese rats in all three groups of animals were matched closely for age and respective body weight. Activity of T4 5'-deiodinase was determined as the rate of T3 production from added T4 under controlled in vitro conditions. Serum T4 and T3 were determined by radioimmunoassay. The rate of T4-to-T3 conversion in BAT was similar in the lean and obese rats maintained at room temperature, whether fed rat chow or a cafeteria diet (approximately 40-50 pmol T3/scapular BAT depot per h). However, expressed per scapular BAT depot, lean rats exposed to cold displayed about a fivefold increase in BAT T3 production (P less than 0.0001), whereas only a small increase was observed in the cold-exposed obese rats. Serum T3 levels tended to be reduced in the Zucker obese rats. Our data indicate a reduced capacity for T3 production in Zucker rat BAT exposed to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acarbose in rats are influenced by the type of dietary starch.

When rats consume a high cornstarch (raw) diet containing the alpha glucosidase inhibitor acarbose, they transport a large portion of the undigested starch into the large bowel, causing massive distention of the lower GI tract. In the present study we compare the effects of acarbose (50 mg per 100 g diet) when mixed in a raw cornstarch diet to its effects when mixed in a cooked cornstarch diet of otherwise identical composition. Controls received the respective diets but without the drug. In contrast to its effects when mixed in the raw cornstarch, mixed in the cooked cornstarch diet, acarbose consumption was not accompanied by any significant fecal losses of dietary starch. The intestinal distention induced by the drug was also much smaller in the rats eating the cooked cornstarch than the raw cornstarch. When either diet contained acarbose, fat depot weights were significantly lower than when the diets did not contain the drug. However, the difference was consistently greater with the raw cornstarch diet.

Norepinephrine turnover in brown adipose tissue is stimulated by a single meal.

A single meal stimulates brown adipose tissue (BAT) thermogenesis in rats. In the present study the role of norepinephrine in this thermogenic response was assessed from the rate of its turnover in BAT after a single test meal. For comparison, norepinephrine turnover was determined in the heart and spleen. A total of 48 male Wistar rats (200 g) were trained to eat during two feeding sessions per day. On the experimental day, one group (n = 24) was meal deprived and the other (n = 24) was given a low-protein high-carbohydrate test meal for 2 h. The synthesis inhibition method with alpha-methyl-p-tyrosine was employed to determine norepinephrine turnover from its concentration at four hourly time points after the meal. Tissue concentrations of norepinephrine were determined by radioimmunoassay. Norepinephrine concentration and turnover rate were increased more than threefold in BAT of the meal-fed compared with the meal-deprived rats (P less than 0.001 and P less than 0.005 for concentration and turnover, respectively). Neither were significantly altered by the meal in the heart or spleen. Other measures of turnover kinetics, turnover time and rate constant, were not significantly affected in any of the tissues examined. Our data suggest that norepinephrine mediates a portion of the thermic effect of meals that originate in BAT.

Meal-induced changes in lipoprotein lipase activity in brown fat and other tissues of rats.

Brown fat thermogenesis is increased after a single test meal. This study was conducted to determine whether lipoprotein lipase activity is higher in brown adipose and other tissues after a single large meal. Rats were trained to eat two large meals per day. Two hours after consuming a test meal, lipoprotein lipase activity was measured in interscapular brown adipose tissue, retroperitoneal and epididymal white adipose tissue, gastrocnemius and soleus skeletal muscles and heart. After a high carbohydrate test meal, lipoprotein lipase activity in white adipose tissue pads was higher (P less than 0.05) and that in brown adipose tissue was lower (P less than 0.05) than in these tissues from the meal-deprived group. Muscle lipoprotein lipase did not change significantly. A high fat test meal did not significantly alter lipoprotein lipase activity in brown adipose tissue, white adipose tissue, gastrocnemius or soleus when compared to the meal-deprived control, but heart lipoprotein lipase activity was significantly elevated. These findings indicate that after a single test meal lipoprotein lipase activity in brown adipose tissue is not higher than that from the meal-deprived group and therefore, lipoprotein lipase may not play a rate-limiting role in moving free fatty acids into this tissue in the postprandial state.

Guanosine diphosphate binding to brown adipose tissue mitochondria is increased after single meal.

A single meal results in an increased thermic activity of brown adipose tissue (BAT). The purpose of the present studies was threefold: 1) to identify major metabolic origins involved in this thermic response, 2) to determine the effect of meal composition on it, and 3) to determine time changes in postprandial brown fat thermogenesis. Wistar rats were trained to eat during 2 feeding sessions/day. On the days of the experiment, rats received a test meal for 2 h, and respective control rats were simultaneously meal deprived. The animals were killed at one or more time points after meal onset, and their BAT was removed for determination of mitochondrial guanosine diphosphate (GDP) binding to indicate rate of uncoupled respiration (expts 1 and 3) or Na+-K+-ATPase activity representing coupled respiration (expt 2). Meal taking was followed by an 85% increase in GDP binding (P less than 0.001). In contrast, Na+-K+-ATPase activity was not altered by a test meal of a similar composition. The largest meal-induced rise in mitochondrial GDP binding was evident during the early postprandial hours, and it was greatly reduced by 10 h after meal onset. Expressed per total interscapular brown fat depot, a high-carbohydrate meal caused a greater increase in GDP binding than an equicaloric high-fat meal. Our data indicate that the BAT proton conductance pathway is activated by a single meal.

Meal-induced brown fat thermogenesis and thyroid hormone metabolism in rats.

The relationship between the meal-induced increase in brown adipose tissue (BAT) thermogenesis, determined by the level of GDP binding to BAT mitochondria, and thyroid hormone metabolism have been examined. A single low-protein, high-carbohydrate meal resulted in a significant increase in the thermogenic activity of BAT. This effect on BAT thermogenesis was accompanied by significant increases in activity of thyroxine 5'-monodeiodinase in the BAT (P less than 0.05) and liver (P less than 0.02) but not with any significant changes in serum concentrations of the thyroid hormones. The stimulatory effects of the meal on BAT thermogenesis and hepatic thyroxine (T4) to triiodothyronine (T3) conversion persisted at least as late as 24 h after meal onset. Food deprivation for 40 h was associated with large reductions in serum concentrations of T3 (P less than 0.01) and T4 (P less than 0.001), but deprivation for 18 h had no significant effect on serum T3 and T4 concentrations. Our data indicate that the meal-induced increase in BAT thermogenesis can be independent from changes in serum concentrations of thyroid hormones and suggest that T3 produced in BAT in response to feeding may play a role in the thermic response of this tissue to meals.

Guanethidine sympathectomy does not prevent meal-induced increases in the weight or oxygen consumption of brown fat.

The interscapular brown adipose tissue (BAT) of adult rats that were neonatally sympathectomized with guanethidine (GUA) consumed less oxygen but weighed the same as BAT from intact controls. In response to a 2-hr mixed-constituent meal, BAT from sympathectomized and control rats showed similar increases in oxygen uptake and weight. These data suggest that some functions of BAT can be maintained even without sympathetic stimulation.

Blood flow into brown fat of rats is greater after a high carbohydrate than after a high fat test meal.

Postprandial oxygen uptake of whole animals and rate of blood flow into the scapular and cervical brown adipose tissue (BAT) of Osborne-Mendel male rats (200 g) were compared for those receiving a high carbohydrate meal or an equicaloric high fat meal. Blood flow was determined by the use of radiolabeled microspheres injected into the left ventricle of anesthetized animals, 2-3 hours after the test meal. In vivo oxygen uptake was elevated by about 10% (P less than 0.05) and blood flow by more than 100% (P less than 0.05) in the group receiving the high carbohydrate meal compared to the high fat meal. The rate of blood flow into tissues other than brown fat was not significantly altered by the composition of the test meal. These tissues included heart, gastrocnemius and soleus muscles, GI tract and white adipose tissue. Our data suggest that a high carbohydrate meal is more thermogenic than a high fat meal, and that the difference in the magnitude of the thermic effect produced by the two meals is paralleled by a corresponding difference in brown fat thermogenesis.

Regional blood flow in rats after a single low-protein, high-carbohydrate test meal.

It was previously observed that a single low-protein, high-carbohydrate test meal results in increased in vitro thermic activity of brown adipose tissue. In the present study, we have examined whether such a meal increases the in vivo thermic activity, estimated from measurement of the rate of blood flow. With radioactively labeled microspheres, blood flows into brown fat and several other tissues were determined in meal-deprived (n = 11) and meal-fed (n = 11) rats. The microspheres were injected into the heart of anesthetized animals about 2-2.5 h after the test meal, one injection in the resting state and one during maximal norepinephrine stimulation. In the resting state, blood flow per gram tissue more than doubled in the brown fat (P less than 0.05) and was increased more than 50% in the heart (P less than 0.01) of the fed group. Blood flows into liver and retroperitoneal white fat were reduced by 40 (P less than 0.01) and 30%, respectively, in the fed group. During norepinephrine infusion, significant meal-associated increases in blood flow were evident only in brown fat (P less than 0.05) and the soleus muscle (P less than 0.05), whereas a significant decrease was observed in the liver (P less than 0.05). No statistically significant meal-associated changes in norepinephrine-stimulated blood flow were found in the other tissues examined (i.e., heart, gastrocnemius, and diaphragm muscles, kidneys, white fat, spleen, and adrenals). Our in vivo data thus support the view that brown fat plays a role in the thermic effect of a meal.

Effect of prandial glucose on brown fat thermogenesis in rats: possible implications for dietary obesity.

We have previously shown that a single meal results in an increased thermic activity of brown adipose tissue (BAT). In the present study, we examine the importance of the availability of glucose in the test meal and in the incubation medium on the rate of in vitro respiration of BAT. We show that a high glucose test meal results in a significant increase in BAT weight and in its in vitro rate of respiration and that the effect of the high glucose meal on brown fat thermogenesis is significantly greater than that of an equicaloric high fructose meal. These data suggest that a decreased postprandial BAT thermogenesis may contribute to the increased metabolic efficiency and to the obesity reported to be associated with sucrose consumption in the rat. We also show that the reduced in vitro rate of respiration of consumption in the rat. We also show that the reduced in vitro rate of respiration of BAT from meal-deprived rats is largely corrected by the addition of glucose and insulin to the incubation medium.

Cholecystokinin, bombesin and neurotensin in brain tissue from obese animals.

The concentration of cholecystokinin (the octapeptide, CCK-8), bombesin, and neurotensin was measured by radioimmunoassay in the cortex, hypothalamus and diencephalon of brains from lean, genetically obese and hypothalamic (VMH) obese rodents. Highest concentration of CCK-8 was found in the cortex whereas highest concentrations of bombesin and neurotensin were in the hypothalamus. When food was provided ad libitum, there was no difference in concentration of any of these peptides between lean and the respective genetically obese mice (ob/ob) and fatty (fa/fa) rats, or between lean and hypothalamic (VMH lesioned) obese rats. Adrenalectomy, which arrested the progression of obesity in both ob/ob and fatty rats, did not result in significant change in concentration of any of the three peptides studied in comparison with the respective sham-operated animals. Though significant differences in cholecystokinin and bombesin concentrations were detectable in some instances between adrenalectomized lean and adrenalectomized obese rats, these differences did not appear to be related to fall in food intake or slowing of body weight gain. Thus a variety of manipulations which altered the nutritional plane of the experimental rodents was not accompanied by significant changes in brain concentrations of cholecystokinin, bombesin or neurotensin.

Compositional and metabolic changes in brown adipose tissue following a single test meal.

In rats maintained on a scheduled feeding plan, the hypertrophy of brown adipose tissue (BAT) observed after a low-protein/high-carbohydrate single test meal was accompanied by significant changes in the percentage of all major constituents of the tissue. There was a fall in the percentage of water (P less than 0.01), a rise in the percentage of fat (P less than 0.05), and a rise in the percentage of glycogen (P less than 0.001). The largest absolute changes following a meal were in the fat content, which almost doubled, and in the glycogen content, which exhibited about a four-fold increase. Deposition of fat in the BAT following the test meal was accompanied by a three-fold increase in the rate of fatty acid synthesis (P less than 0.05). The in vitro respiration rate of BAT was usually significantly increased in the meal-fed rats, but the effect of replacing the protein content of the test meal with starch was not clear. A lower protein, higher starch diet (9% of calories from protein, 72% from starch) resulted in a trend for a larger thermic effect than a higher protein, lower starch diet (27% of calories from protein, 54% from starch).

Ovarian hormones influence brown adipose tissue.

Adult female rats were ovariectomized (OVX) or sham-operated and 4-5 weeks later OVX groups were treated with estradiol benzoate (EB), progesterone, both hormones, or the oil vehicle. All rats were sacrificed on the 4th day of hormone treatment following an overnight fast and a terminal meal. Interscapular brown adipose tissue (BAT) pads of EB-treated groups were heavier and contained more lipid than those of the other OVX groups. Lipid content of adipose tissue differed according to site (BAT less than inguinal less than parametrial = retroperitoneal), but only BAT exhibited differential responsiveness to hormonal treatments. There was also a trend for increased oxygen consumption by BAT from EB-treated rats. It is concluded that BAT may be involved in the process of increased energy expenditure by estrogen-treated rats.

Physiologic responses to exercise in normal and obese women.

The present study examines the possibility that the reduced activity commonly found in obese individuals could stem from a reduced physiological responsiveness to exercise. Responses to bicycle ergometer exercise (300 kpm/min) of four obese and four normal weight women were observed in a metabolic ward. This resulted in decreases in exercise heart rate and oxygen consumption, indicating an improvement in mechanical efficiency and suggesting an increase in physical working capacity. It also resulted in some decreases of resting oral temperature. The differences in the response to exercise between the obese and the normal weight groups were small and not statistically significant. The normal weight subjects showed a trend for greater decreases in heart rate and O2 consumption during exercise, while in the obese resting oral temperature tended to be more reduced. The results suggest that obesity in our subjects was not related to a deranged physiological response to physical activity.

Inverse relationship between brown fat thermogenesis and meal size: the thermostatic control of food intake revisited.

This study examines a new hypothesis whereby heat production from brown fat in response to eating may serve as a feedback signal for satiety. To test this hypothesis, in vitro respiration rate of brown adipose tissue (BAT) was determined in relation to the voluntary caloric intake of the preceding test meal. This relationship was examined as a function of meal composition and of obesity. It was found that in rats fed a high fat diet, as well as in two types of obese rats (VMH and Zucker), respiration rate per 100 mg tissue was significantly reduced, and energy intake of the preceding test meal increased compared to rats receiving a low fat diet or to respective lean rats. These data lend support to a brown fat mediated thermostatic hypothesis for the control of food intake.