[Food and health: general review].
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Animals↗
Biomedical subjects
J Lupien
Publications and source records attributed to J Lupien.
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.
Adipose Tissue, Brown↗
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.
Adipose Tissue, Brown↗
Dynamic and static phases of obesity following lesions in PVN and VMH.
The effect of electrolytic lesions in the ventromedial hypothalamus (VMH) and the paraventricular nucleus (PVN) has been compared during both the dynamic and static phase of weight gain. Hyperphagia and weight gain were greater in the VMH-lesioned rats than in the PVN-lesioned rats. Food intake increased at night after both lesions but increased in the daytime only in VMH-lesioned rats. During the dynamic phase of rapid weight gain, the diurnal pattern of corticosterone was blunted to a similar degree in both lesioned groups. The morning insulin concentrations were higher in both lesioned groups than in the sham-operated controls, but in the static phase only the VMH-lesioned rats had higher insulin levels. In the afternoon the insulin was higher in the VMH-lesioned rats than in either the sham-operated or PVN-lesioned rats. In the dynamic phase the weight of interscapular brown adipose tissue was significantly increased in the VMH-lesioned rats, but the specific GDP binding was depressed both in the morning and afternoon when compared with either the sham-operated or PVN-lesioned groups. In both the dynamic and static phases GDP binding was similar in sham-operated and PVN-lesioned animals. The differences in concentration of corticosterone in morning and afternoon were smaller in the lesioned groups than in the controls. These data are consistent with the hypothesis that animals with PVN lesions do not show the disturbances in food intake or in the autonomic nervous system that characterize the VMH-lesioned rats.
Adipose Tissue, Brown↗
Intensive exercise training does not improve intravenous glucose tolerance in severely diabetic rats.
Several studies have recently demonstrated that exercise training improves glucose tolerance in mildly diabetic rats. To test whether some minimal levels of circulating insulin are required to observe the beneficial effects of exercise training, severe diabetes was induced by injecting female Wistar rats with streptozotocin. Half of diabetic and control rats were submitted to a strenuous program of swimming exercise. After 4 wks of training, intravenous glucose tolerance tests (IVGTT) were performed in precannulated, unrestrained and unanesthetized animals. In non-diabetic rats, exercise training significantly reduced both basal and glucose-stimulated levels of insulin (P less than 0.01) without altering glucose tolerance. On the other hand, the same training program applied to severely diabetic animals (basal plasma insulin levels less than 8 microU/ml) failed to reduce the marked hyperglycemia in the resting state (400 mg% range) as well as during the entire IVGTT (400-500 mg%). The results indicate that exercise training effectively increased the sensitivity of peripheral tissues to insulin in non-diabetic but not in diabetic animals. The data also suggest that a minimal amount of circulating insulin is required in order to observe the beneficial effects of exercise training.
Adipose Tissue↗
Synergistic improvement of glucose tolerance by sucrose feeding and exercise training.
The interactive effects of exercise training (5-7 wk) and sucrose consumption (ad libitum feeding of a 32% sucrose solution and Purina chow) on intravenous glucose tolerance and plasma insulin levels were investigated using a 2 X 2 experimental design. Rats were divided in Purina-sedentary, Purina-trained, sucrose-sedentary, and sucrose-trained groups. Sucrose feeding of sedentary animals significantly increased basal and glucose-stimulated insulin levels and improved basal glycemia and glucose tolerance. On the other hand, exercise training of Purina-fed animals significantly reduced basal as well as glucose-stimulated insulinemia without altering basal glycemia or glucose tolerance. Such a sparing effect of exercise training on insulin requirements was not as evident in rats consuming sucrose. These animals displayed a reduced basal glycemia (P less than 0.01) with normal basal insulin levels. Their glucose tolerance was markedly improved (P less than 0.01) but their insulin response during intravenous glucose tolerance test remained as high as in sucrose-sedentary animals. Results from these studies indicate that sucrose feeding of sedentary animals leads to hyperinsulinemia without compensatory insulin resistance, resulting in an improvement of glucose tolerance, exercise training increases the sensitivity of peripheral tissues to insulin, and the marked improvement of glucose tolerance observed in sucrose-trained animals results from a synergistic combination of the above two factors, i.e., increased insulinemia (induced by diet) and enhanced insulin sensitivity (induced by training).
Adipose Tissue↗
Cold exposure reverses the diabetogenic effects of high-fat feeding.
Long-term cafeteria feeding, cold exposure, and the combination of treatments increased energy intake in female Wistar rats by 25%, 113%, and 150%, respectively, in comparison with controls (P less than 0.01). Although cafeteria feeding at room temperature markedly increased the insulin response to an intravenous glucose tolerance test (IVGTT), glucose tolerance was deteriorated (P less than 0.01). In contrast, cold exposure significantly improved glucose tolerance in the presence of a reduced insulin response in Purina- and cafeteria-fed animals. Moreover, cold exposure also decreased body weight gain and increased brown adipose tissue mass, total cytochrome-oxidase activity, and cellularity by approximately 600-800%. The results suggest that cold exposure enhances insulin sensitivity of peripheral tissues, whereas hyperphagia on a high-fat, low-protein diet leads to insulin resistance. In addition, the results demonstrate that prolonged stimulation of energy expenditure by cold exposure not only reverses the diabetogenic effects of cafeteria feeding but also improves glucose tolerance. This phenomenon could result from a combination of two factors: (1) a cold-induced prevention of obesity; and (2) an enhanced disposal of circulating glucose into peripheral tissues, including brown adipose tissue.
Adipose Tissue↗
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.
Adipose Tissue, Brown↗
Interaction of light and corticosterone on food intake and brown adipose tissue of the rat.
The food intake of sham-operated and adrenalectomized rats was measured in 12-h intervals with animals housed in either alternating periods of 12:12 light-dark or in continuous light. The food intake with alternating light and dark was unaffected by adrenalectomy. The maintenance of a constant infusion of corticosterone in adrenalectomized rats also did not disturb the pattern of food intake. In continuous light, food intake was not significantly different in each 12-h period of the daily cycle. Neither adrenalectomy nor the injection of corticosterone, 240 micrograms/day, altered the average 12-h food intake in rats in constant light. The weight of interscapular brown adipose was smaller in adrenalectomized animals, but the protein content was unaffected. Adrenalectomy significantly increased the specific binding of the purine nucleotide GDP to mitochondria from brown adipose tissue. This specific binding was restored to normal by either corticosterone infusion or injection. We conclude that light is the principal entrainer for the average food intake during 12-h periods and that within the framework of these experiments corticosterone plays an insignificant role in controlling food intake. However, adrenalectomy did significantly increase the purine nucleotide binding to mitochondria from brown adipose tissue.
Adipose Tissue, Brown↗
Interactions of cold exposure and starvation on glucose tolerance and insulin response.
The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. "Accelerated starvation" induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15-18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.
Acclimatization↗
Effects of sucrose, caffeine, and cola beverages on obesity, cold resistance, and adipose tissue cellularity.
Rats consuming Coca-Cola and Purina chow ad libitum increased their total energy intake by 50% without excess weight gain. Their resistance to cold was markedly improved. These phenomena were characterized by significant increases in interscapular brown adipose tissue weight (IBAT) (91%), cellularity (59%), triglyceride content (52%), protein content (94%), and cytochrome oxidase activity (167%). In contrast, Coca-Cola consumption did not significantly affect the cellularity or triglyceride content of parametrial white adipose tissue (PWAT), although it slightly augmented PWAT weight. The effects of Coca-Cola on cold resistance, IBAT cellularity, and composition were entirely reproduced by sucrose, but not caffeine, consumption. Although caffeine also increased IBAT cellularity and composition, it significantly decreased the rate of body weight gain, PWAT weight, and adipocyte size. Moreover, it markedly inhibited adipocyte proliferation in PWAT thereby mimicking the effects of exercise training and food restriction (Bukowiecki et al., Am. J. Physiol. 239 (Endocrinol. Metab. 2): E422-E429, 1980). It is concluded a) that sucrose and Coca-Cola consumption improve the resistance of rats to cold, most probably by increasing brown adipose tissue cellularity, and b) that moderate caffeine intake might be useful for inhibiting proliferative activity in white adipose tissue, thereby preventing obesity.
Adipose Tissue↗
Morphology and metabolism of human fat cells: a reliability study.
Twenty-three male subjects, 31.7 (mean) +/- 7.4 (s.d.) yr of age, weight 70.7 +/- 9.0 kg and with 13.4 +/- 4.7 percent body fat were submitted twice within a week to biopsies of subcutaneous adipose tissue in the suprailiac region. Two biopsies (sample A and B) were obtained on day 1 and two others (sample C and D) in the contralateral region on day 2. Average fat cell diameter (ACD) was assessed by measuring at least 500 cells per subject. There was no significant difference between day 1 and day 2 for ACD (means 1 = 62.6 +/- 12.2 micron; means 2 = 63.2 +/- 12.3 micron). Intra-class reliability coefficient reached 0.97. ANOVA-RBFD showed no day or sample effects (P greater than 0.05) on ACD. Basal (BL), epinephrine submaximal (10(-5) M) (ESML) and epinephrine maximal (10(-4) M) (EML) stimulated lipolysis have been determined for 18 of these subjects. Intra-class reliabilities were moderately high, reaching 0.71 for BL, 0.83 for ESML and 0.72 for EML, respectively. Controlling the level of activity for 36 h prior to the biopsies resulted, however, in increased coefficients. In this case, intra-class coefficients computed with 11 subjects were 0.99 for BL, 0.88 for ESML and 0.85 for EML. The data demonstrate that ACD and lipolytic capacity can be reliably measured, particularly when activity of subjects is controlled during the 36-h period preceding the biopsies.
Adipose Tissue↗
Metabolic relationships between lipolysis and respiration in rat brown adipocytes. The role of long chain fatty acids as regulators of mitochondrial respiration and feedback inhibitors of lipolysis.
The calorigenic action of norepinephrine in isolated brown adipocytes was selectively mimicked by theophylline, dibutyryl cyclic AMP, and the principal fatty acids known to be present in the acyl moieties of brown adipose tissue triglycerides (palmitic, oleic, and linoleic acids). The stimulatory effects of fatty acids were entirely reversible, occurred at physiological concentrations, and were critically dependent upon the molar ratio of extracellular fatty acids to albumin. The calorigenic potency of fatty acids increased with their chain length. The apparent synchrony between the switching "on and off" of lipolysis and respiration by norepinephrine and propranolol indicated that the two phenomena are functionally inter-related and that they are both mediated by beta-adrenoreceptors. Respiratory stimulation by palmitic acid was accompanied by an inhibition of glycerol release suggesting that fatty acids retroinhibit lipolysis while simultaneously activating respiration. Studies with 2-tetradecylglycidic acid, oligomycin, and uncouplers of oxidative phosphorylation support the view that fatty acids exert their calorigenic effects by increasing mitochondrial proton permeability and by simultaneously serving as substrates for beta-oxidation via carnitine-dependent pathways. Since fatty acids mimicked the calorigenic action of norepinephrine even when beta-adrenoreceptors were blocked by propranolol, it is concluded that cyclic AMP controls respiration indirectly, most probably by modulating lipolysis. It is suggested that endogenous long chain fatty acids released in consequence of cyclic AMP activation of lipolysis play a fundamental role in the control of brown adipose tissue metabolism by self-regulating lipolysis and by serving as physiological modulators of mitochondrial oxygen consumption.
Adipose Tissue, Brown↗
Mechanism of enhanced lipolysis in adipose tissue of exercise-trained rats.
The effects of exercise training and food restriction on the regulation of lipolysis were studied comparatively in adipocytes isolated from male and female rats. Exercise training inhibited cell proliferation in parametrial, but not in epididymal adipose tissue, whereas it significantly reduced adipocyte size in both fat depots. Adipocyte capacity for responding lipolytically to epinephrine (10 microns) or to ACTH (1 micron) was markedly increased by exercise training. Enhanced lipolysis was also observed when cells isolated from exercise-trained animals were stimulated by bypassing with dibutyryl cyclic AMP (5 mM) or theophylline (5 mM) the early metabolic steps associated with hormonal activation of the adenylate cyclase complex. Significantly, binding of (-)-[3H]dihydroalprenolol to cellular receptor sites was not affected by exercise training. It is therefore concluded that exercise training increases adipocyte responsiveness to lipolytic hormones at a metabolic step distal to stimulus recognition by adrenoreceptors, possibly at the level of protein kinases or lipases. Food restriction markedly reduced adipocyte size and partially mimicked the effects of exercise training on adipocyte proliferation and lipolysis.
Adipose Tissue↗