Arginine-induced pancreatic hormone secretion during exercise in rats

Trabelsi, Fethi, and Jean-Marc Lavoie. Arginine-inducedpancreatic hormone secretion during exercise in rats.J. Appl. Physiol. 81(6):2528-2533, 1996.The aim of the present investigation was to1) determine whetherarginine-induced pancreatic hormone secretion can be modified during anexercise bout, and 2) verify whetherthe sectioning of the hepatic branch of the vagus nerve can alter thearginine-induced insulin and glucagon secretion during exercise inrats. To this end, we studied the effects of an intraperitonealinjection of arginine (1 g/kg body mass) during an exercise bout (30 min, 26 m/min, 0% grade) on the pancreatic hormone responses. Theseeffects were determined in one group of sham-operated exercising ratsand compared with three control groups: one group of resting rats, onegroup of saline-injected exercising rats, and one group ofhepatic-vagotomized exercising rats. Five minutes after the injectionof arginine, significant (P < 0.05)increases in insulin, glucagon, and C-peptide concentrations wereobserved in exercising as well as in resting rats. These responses werenot, however, altered by the hepatic vagotomy and/or by theexercise bout. It is concluded that arginine is a potent stimulus ofpancreatic hormone secretion during exercise, even though thesympathoadrenal system is activated. These results also indicate that ahepatic vagotomy does not seem to influence arginine-inducedhormonal pancreatic responses and question the role of the putativehepatic arginoreceptors in the control of the pancreatic hormonesecretion during exercise.

     

Effects of supramaximal exercise on blood glucose levels during a subsequent exercise

The purpose of the present investigation was to examine the effects of hyperglycemia induced by supramaximal exercise on blood glucose homeostasis during submaximal exercise following immediately after. Six men were subjected to three experimental situations; in two of these situations, 3 min of high-intensity exercise (corresponding to 112, SD 1% VO2max) was immediately followed by either a 60-min period of submaximal exercise (68, SD 2% VO2max) or a 60-min resting period. In the third situation, subjects performed a 63-min period of submaximal exercise only. There were no significant differences between the heart rates, oxygen uptakes, and respiratory exchange ratios during the two submaximal exercise bouts (greater than 15 min) whether or not preceded by supramaximal exercise. The supramaximal exercise was associated within 10 min of the start increases (P less than 0.05) in blood glucose, insulin, and lactate concentrations. This hyperglycemia was more pronounced when subjects continued to exercise submaximally than when they rested (at 7.5 min; P less than 0.05). There was a more rapid return to normal exercise blood glucose and insulin values during submaximal exercise compared with rest. The data show that the hyperinsulinemia following supramaximal exercise is corrected in between 10-30 min during submaximal exercise following immediately, suggesting that this exercise combination does not lead to premature hypoglycemia.     

Effect of naloxone on pancreatic and gastric endocrine function in response to carbohydrate and fat-rich test meals

The present study was designed to determine the effect of naloxone, a specific opiate receptor antagonist, on postprandial levels of insulin, glucagon, pancreatic polypeptide (PP), somatostatin-like immunoreactivity (SLI) and gastrin in response to carbohydrate and fat-rich test meals in a group of 6 healthy volunteers. The addition of naloxone to a meal consisting of 50 g sucrose dissolved in 200 ml water augmented the rise of plasma insulin levels significantly during the first 30 min after its ingestion and reduced the decrease of plasma glucagon. During the ingestion of a fat-rich meal in form of 200 ml cream naloxone reduced the rise in plasma insulin and pancreatic polypeptide and elevated glucagon levels during the last 30 min of the experimental period. When sucrose was dissolved in 200 ml cream the addition of naloxone augmented the postprandial rise of insulin levels between 15 and 60 min after ingestion of the meal and elicited an increase of plasma SLI and PP levels throughout the entire experimental period which indicates that post-prandial levels of insulin, glucagon, PP and SLI are modulated via endogenous opiate receptors during the ingestion of carbohydrate and fat test meals and that this effect depends on the composition of the ingested nutrients. These data raise the possibility that endogenous opiates participate in the regulation of postprandial insulin, glucagon, somatostatin and pancreatic polypeptide release not only in certain disease states as demonstrated recently for insulin secretion in type II diabetes mellitus but endogenous opiates may also be of importance under physiological conditions.     

Intraportal GLP-1 infusion increases nonhepatic glucose utilization without changing pancreatic hormone levels

After a meal, glucagon-like peptide-1 (GLP-1) levels in the hepatic portal vein are elevated and are twice those in peripheral blood. The aim of this study was to determine whether any of GLP-1's acute metabolic effects are initiated within the hepatic portal vein. Experiments consisted of a 40-min basal period, followed by a 240-min experimental period, during which conscious 42-h-fasted dogs received glucose intraportally (4 mgxkg(-1)xmin(-1)) and peripherally (as needed) to maintain arterial plasma glucose levels at approximately 160 mg/dl. In addition, saline was given intraportally (CON; n = 8) or GLP-1 (1 pmolxkg(-1)xmin(-1)) was given into the hepatic portal vein (POR; n = 11) or the hepatic artery (HAT; n = 8). Portal vein plasma GLP-1 levels were basal in CON, 20x basal in POR, and 10x basal in HAT, whereas levels in the periphery and liver were the same in HAT and CON. The glucose infusion rate required to maintain hyperglycemia was significantly greater in POR (8.5 +/- 0.7 mgxkg(-1)xmin(-1), final 2 h) than in either CON or HAT (6.0 +/- 0.5 or 6.7 +/- 1.0 mgxkg(-1)xmin(-1), respectively). There were no differences among groups in either arterial plasma insulin (24 +/- 2, 23 +/- 3, and 23 +/- 3 microU/ml for CON, POR, and HAT, respectively) or glucagon (23 +/- 2, 30 +/- 3, and 25 +/- 2 pg/ml) levels during the experimental period. The increased need for glucose infusion reflected greater nonhepatic as opposed to liver glucose uptake. GLP-1 infusion increased glucose disposal independently of changes in pancreatic hormone secretion but only when the peptide was delivered intraportally.     

Beta-endorphin, adrenocorticotropic hormone, cortisol and catecholamines during aerobic and anaerobic exercise

Twelve non-specifically trained volunteers (aged 26.5 years, SD 3.6) performed exhausting incremental graded exercise (ST) and 1-min anaerobic cycle ergometer exercise (AnT) at 2-h intervals for the purpose of investigating beta-endorphin (beta-E) behaviour dependent on exercise intensity and anaerobic metabolism. In order to determine [beta-E], adrenocorticotropic hormone [ACTH], cortisol [C], adrenaline [A] and noradrenaline [NA] concentrations, venous blood samples were collected prior and subsequent to exercise until the 20th min of the recovery period, as well as in ST before and after exceeding the individual anaerobic threshold (THan,i). Before, during and after ST, lactate concentration, heart rate and perceived degree of exertion were also determined; after AnT maximum lactate concentration was measured. Both types of exercise led to significant increases in [beta-E], [ACTH], [A] and [NA], with levels of [beta-E] and [ACTH] approximately twice as high after ST as after AnT. The [C] increased significantly only after ST. During ST significant changes in [beta-E] and [ACTH] were measured only after exceeding THan,i. At all measuring times before and after ST and AnT both hormones correlated positively. In AnT the increases of [beta-E] and [A] demonstrated a correlation (r = 0.65; P less than 0.05). Both in AnT and ST there was a relationship between the maximum concentrations of beta-E and lactate (r = 0.63 and 0.71; each P less than 0.05). We therefore conclude that physical exercise with increasing or mostly anaerobic components leads to an increase in [beta-E], the extent correlating with the degree of lactate concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of dietary manipulations and glucose infusion on glucagon response during exercise in rats

Tadjoré, Maurice, Raynald Bergeron, Martin Latour,François Désy, Claude Warren, and Jean-Marc Lavoie.Effects of dietary manipulations and glucose infusion on glucagonresponse during exercise in rats. J. Appl.Physiol. 83(1): 148-152, 1997.The purpose of thepresent investigation was to test the hypothesis that blood glucoseconcentration is not always related to glucagon response duringexercise. Three groups of rats were submitted to a prolonged (3-h)swimming exercise. Two groups of rats had their normal food intakerestricted by 50% the night before the experiment. One of these twogroups of rats was intravenously infused with glucose throughoutexercise to maintain euglycemia. The third group of rats swam whileunder normal dietary conditions. Plasma glucose, sampled in arterialblood, was reduced (P < 0.05) at 75, 105, 150, and 170 min of exercise (from ~130 to 110 mg/dl) in thefood-restricted animals without glucose infusion, whereas a significant(P < 0.05) increase was measured inthe two other groups during exercise. A significant(P < 0.01) difference in the meanintegrated areas under the glucose-concentration curve was found onlybetween the fed and the two food-restricted groups. Plasma insulinconcentrations decreased (P < 0.05)similarly in all groups during exercise, whereas plasma epinephrine andnorepinephrine concentrations increased significantly(P < 0.01) in all groups. Despitedifferences between groups in plasma glucose response during exercise,and despite the absence of any decrease in exercising blood glucoselevels in at least two of the three groups, plasma glucagon responseswere increased (P < 0.05) similarlyin all groups (from ~250 to 550 pg/ml) at the end of the exerciseperiod. The increase in glucagon was significant after 90 min ofexercise in the food-restricted groups, with or without glucoseinfusion, but only after 140 min in the fed group. These resultsindicate that the glucagon response during exercise is not alwayslinked to the decrease in plasma glucose.

     

Beta-endorphin and ACTH levels in peripheral blood during and after aerobic and anaerobic exercise

Beta-endorphin (beta-End) and adrenocorticotrophic hormone (ACTH) were determined in the peripheral blood of 14 human volunteers exercising on a bicycle ergometer. After 1 h of submaximal work below anaerobic threshold (AT), defined as the 4 mmol X l-1 lactic acid level in arteriolar blood (Kindermann 1979; Mader 1980), beta-End and ACTH levels did not change from control conditions. Eleven of the same 14 subjects performed an uninterrupted graded exercise test on the same bicycle ergometer until exhaustion. This time beta-End and ACTH levels increased concomitantly with exercise of high intensity: at each moment, during and after this maximal test, a highly significant correlation (P less than 0.0001) was noted between the levels of beta-End and ACTH. The peak values of these hormones were reached within 10 min after stopping maximal exercise, and coincided with lactic acid peak levels. A rise in lactic acid levels above the anaerobic threshold always preceded the exercise-induced rise in beta-End and ACTH. Within the population tested, two subgroups could be distinguished: one comprising individuals whose hormonal response nearly coincided with the rise in lactic acid (rapid responders) and a second group composed of subjects whose normal response appeared delayed with respect to the lactic acid rise (slow responders). These results support the view that beta-End and ACTH are secreted in equimolar quantities into the blood circulation in response to exercise, and suggest that metabolic changes of anaerobiosis play a key role in the regulation of stress-hormone release.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of hypophysectomy on pancreatic islet hormone and insulin-like growth factor I content and mRNA expression in rat

The growth arrest after hypophysectomy in rats is mainly due to growth hormone (GH) deficiency because replacement of GH or insulin-like growth factor (IGF) I, the mediator of GH action, leads to resumption of growth despite the lack of other pituitary hormones. Hypophysectomized (hypox) rats have, therefore, often been used to study metabolic consequences of GH deficiency and its effects on tissues concerned with growth. The present study was undertaken to assess the effects of hypophysectomy on the serum and pancreatic levels of the three major islet hormones insulin, glucagon, and somatostatin, as well as on IGF-I. Immunohistochemistry (IHC), in situ hybridization (ISH), radioimmunoassays (RIA), and Northern blot analysis were used to localize and quantify the hormones in the pancreas at the peptide and mRNA levels. IHC showed slightly decreased insulin levels in the cells of hypox compared with normal, age-matched rats whereas glucagon in cells and somatostatin in cells showed increase. IGF-I, which localized to cells, showed decrease. ISH detected a slightly higher expression of insulin mRNA and markedly stronger signals for glucagon and somatostatin mRNA in the islets of hypox rats. Serum glucose concentrations did not differ between the two groups although serum insulin and C-peptide were lower and serum glucagon was higher in the hypox animals. These changes were accompanied by a more than tenfold drop in serum IGF-I. The pancreatic insulin content per gram of tissue was not significantly different in hypox and normal rats. Pancreatic glucagon and somatostatin per gram of tissue were higher in the hypox animals. The pancreatic IGF-I content of hypox rats was significantly reduced. Northern blot analysis gave a 2.6-, 4.5-, and 2.2-fold increase in pancreatic insulin, glucagon, and somatostatin mRNA levels, respectively, in hypox rats, and a 2.3-fold decrease in IGF-I mRNA levels. Our results show that the fall of serum IGF-I after hypophysectomy is accompanied by a decrease in pancreatic IGF-I peptide and mRNA but by partly discordant changes in the serum concentrations of insulin and glucagon and the islet peptide and/or mRNA content of the three major islet hormones. It appears that GH deficiency resulting in a low IGF-I state affects translational efficiency of these hormones as well as their secretory responses. The maintenance of normoglycemia in the presence of reduced insulin and elevated glucagon serum levels, both of which would be expected to raise blood glucose, may result mainly from the enhanced insulin sensitivity, possibly due to GH deficiency and the subsequent decrease in IGF-I production.     

IGF alters jejunal glucose transporter expression and serum glucose levels in immature rats

Milk-borne insulin-like growth factors (IGFs) enhance nutrient absorption in the immature intestine, which is characterized by low levels of glucose oxidation. We therefore hypothesized that feeding a rat milk substitute (RMS) devoid of growth factors to rat pups would lower serum glucose levels relative to dam-fed control rats and that supplementation of RMS with physiological doses of either IGF-I or IGF-II would normalize serum glucose levels via increased jejunal glucose transporter 2 (GLUT2) and high-affinity Na(+)-glucose cotransporter (SGLT1) expression. We found lower serum glucose concentrations in RMS-fed pups; in contrast, serum glucose levels in the IGF-supplemented pups were similar to those of dam-fed controls. RT-PCR and laser scanning confocal microscopy similarly demonstrated that IGF supplementation increased expression of jejunal glucose transporters. Further experiments demonstrated that IGF supplementation altered mRNA levels of key mitochondrial enzymes without altering jejunal lactase activity. We conclude that IGF-I and IGF-II supplementation increases serum glucose levels in the immature rat pup fed artificial formula and alters gene expression of the jejunal glucose transporters.     

Partial hepatectomy alters serum hormone levels in rats.

The level of thyroid stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), thyroxine (T4), 3,5,3'-L-triiodothyronine (T3), corticosterone, testosterone and insulin in serum were measured at 1, 12, 48 and 120 h after partial hepatectomy (PH) or sham operation in rats. After PH the level of ACTH and corticosterone was significantly elevated while that of TSH, T4 and testosterone was decreased and returned to the values found in sham operated animals within 5 days. The level of T3 was unchanged. These results show an increase in the function of pituitary-adrenal axis and a decrease in that of pituitary-thyroid axis shortly following PH with the tendency to return to normal function within five days.     

Intraportal glucose infusion and pancreatic islet blood flow in anesthetized rats

The aim of the study was to evaluate whether a selective increase in portal vein blood glucose concentration can affect pancreatic islet blood flow. Anesthetized rats were infused (0.1 ml/min for 3 min) directly into the portal vein with saline, glucose, or 3-O-methylglucose. The infused dose of glucose (1 mg. kg body wt(-1). min(-1)) was chosen so that the systemic blood glucose concentration was unaffected. Intraportal infusion of D-glucose increased insulin release and islet blood flow; the osmotic control substance 3-O-methylglucose had no such effect. A bilateral vagotomy performed 20 min before the infusions potentiated the islet blood flow response and also induced an increase in whole pancreatic blood flow, whereas the insulin response was abolished. Administration of atropine to vagotomized animals did not change the blood flow responses to intraportal glucose infusions. When the vagotomy was combined with a denervation of the hepatic artery, there was no stimulation of islet blood flow or insulin release after intraportal glucose infusion. We conclude that a selective increase in portal vein blood glucose concentration may participate in the islet blood flow increase in response to hyperglycemia. This effect is probably mediated via periarterial nerves and not through the vagus nerve. Furthermore, this blood flow increase can be dissociated from changes in insulin release.     

Silymarin induces recovery of pancreatic function after alloxan damage in rats

Alloxan has been widely used to produce experimental diabetes mellitus syndrome. This compound causes necrosis of pancreatic beta-cells and, as is well known, induces oxidant free radicals which play a relevant role in the etiology and pathogenesis of both experimental and human diabetes mellitus. Previously we have reported hypoglycemic and antilipoperoxidative actions of silymarin in serum and pancreatic tissue respectively. The aim of this study was to test whether silymarin could reduce the hyperglycemia and revert the pancreatic damage in alloxan treated rats, tested with silymarin in two protocols: using both compounds simultaneously for four or eight doses, or using the compound 20 days after alloxan administration for 9 weeks. Serum glucose and insulin were determined, and pancreatic fragments were used for histology and insulin immunohistochemistry. Pancreatic islets were isolated to assess insulin and Pdx1 mRNA expression by RT-PCR. Our results showed that 72 hours after alloxan administration, serum glucose increased and serum insulin decreased significantly, whereas pancreatic tissue presented morphological abnormalities such as islet shrinkage, necrotic areas, loss of cell organization, widespread lipoid deposits throughout the exocrine tissue, and loss of beta cells, but insulin and glucagon immunoreactivity was scattered if any. In contrast the pancreatic tissue and both insulin and glucose serum levels of rats treated with silymarin were similar to those of control animals. In addition, insulin and glucagon immunoreactive cells patterns in Langerhans islets were also normal, and normal insulin and Pdx1 mRNA expression patterns were detected during pancreatic recovery in Langerhans islets. The overall results suggest that silymarin induces pancreatic function recovery demonstrated by insulin and glucagon expression protein and normoglycemia after alloxan pancreatic damage in rats.     

Interactive effect of exercise training and growth hormone administration on glucose tolerance and muscle GLUT4 protein expression in rats

The insulin-resistance effect of growth hormone (GH) administration has been frequently reported. The present study investigated the effect of GH administration on glucose tolerance and muscle GLUT4 protein expression in exercise-trained and untrained rats. Forty-eight rats were weight-matched and assigned to the following 4 groups: control, GH, exercise training, and exercise training + GH groups. After 2 weeks of GH injections (65 µg/kg/day) and exercise training, the glucose tolerance and insulin response were measured in these rats. The GLUT4 protein level, glycogen storage, and citrate synthase activity were determined in red gastrocnemius and plantaris muscles. Daily GH administration elevated the curves of the oral glucose tolerance test and insulin response compared with those of saline-injected control rats. Furthermore, exercise training completely eliminated this GH-induced insulin resistance as determined 18 h after the last bout of exercise training. Additionally, exercise training significantly increased muscle glycogen storage and GLUT4 protein levels. GH administration did not affect the GLUT4 protein and glycogen storage increases induced by exercise training, but the citrate synthase activity in the plantaris muscle was further elevated by GH administration to a level above that induced by training. In conclusion, this is the first study that demonstrates that regular exercise training prevents GH-induced insulin-resistance side effect in rats.     

Blockade of IRS1 in isolated rat pancreatic islets improves glucose-induced insulin secretion

Several neural, hormonal and biochemical inputs actively participate in the balance of insulin secretion induced by blood glucose fluctuations. The exact role of insulin as an autocrine and paracrine participant in the control of its own secretion remains to be determined, mostly due to insufficient knowledge about the molecular phenomena that govern insulin signaling in pancreatic islets. In the present experiments we demonstrate that higher insulin receptor and insulin receptor substrates-1 and -2 (IRS1 and IRS2) concentrations are predominantly encountered in cells of the periphery of rat pancreatic islets, as compared to centrally located cells, and that partial blockade of IRS1 protein expression by antisense oligonucleotide treatment leads to improved insulin secretion induced by glucose overload, which is accompanied by lower steady-state glucagon secretion and blunted glucose-induced glucagon fall. These data reinforce the inhibitory role of insulin upon its own secretion in isolated, undisrupted pancreatic islets.     

GLUT2 in pancreatic and extra-pancreatic gluco-detection

Detection of variations in blood glucose concentrations by pancreatic &#103 -cells and a subsequent appropriate secretion of insulin are key events in the control of glucose homeostasis. Because a decreased capability to sense glycemic changes is a hallmark of type 2 diabetes, the glucose signalling pathway leading to insulin secretion in pancreatic &#103 -cells has been extensively studied. This signalling mechanism depends on glucose metabolism and requires the presence of specific molecules such as GLUT2, glucokinase and the K ATP channel subunits Kir6.2 and SUR1. Other cells are also able to sense variations in glycemia or in local glucose concentrations and to modulate different physiological functions participating in the general control of glucose and energy homeostasis. These include cells forming the hepatoportal vein glucose sensor, which controls glucose storage in the liver, counterregulation, food intake and glucose utilization by peripheral tissues and neurons in the hypothalamus and brainstem whose firing rates are modulated by local variations in glucose concentrations or, when not protected by a blood-brain barrier, directly by changes in blood glucose levels. These glucose-sensing neurons are involved in the control of insulin and glucagon secretion, food intake and energy expenditure. Here, recent physiological studies performed with GLUT2 -/- mice will be described, which indicate that this transporter is ess ential for glucose sensing by pancreatic &#103 -cells, by the hepatoportal sensor and by sensors, probably located centrally, which control activity of the autonomic nervous system and stimulate glucagon secretion. These studies may pave the way to a fine dissection of the molecular and cellular components of extra-pancreatic glucose sensors involved in the control of glucose and energy homeostasis.     

L-Arginine infusion increases glucose clearance during prolonged exercise in humans

Nitric oxide synthase (NOS) inhibition has been shown in humans to attenuate exercise-induced increases in muscle glucose uptake. We examined the effect of infusing the NO precursor L-arginine (L-Arg) on glucose kinetics during exercise in humans. Nine endurance-trained males cycled for 120 min at 72+/-1% Vo(2 peak) followed immediately by a 15-min "all-out" cycling performance bout. A [6,6-(2)H]glucose tracer was infused throughout exercise, and either saline alone (Control, CON) or saline containing L-Arg HCL (L-Arg, 30 g at 0.5 g/min) was confused in a double-blind, randomized order during the last 60 min of exercise. L-Arg augmented the increases in glucose rate of appearance, glucose rate of disappearance, and glucose clearance rate (L-Arg: 16.1+/-1.8 ml.min(-1).kg(-1); CON: 11.9+/- 0.7 ml.min(-1).kg(-1) at 120 min, P<0.05) during exercise, with a net effect of reducing plasma glucose concentration during exercise. L-Arg infusion had no significant effect on plasma insulin concentration but attenuated the increase in nonesterified fatty acid and glycerol concentrations during exercise. L-Arg infusion had no effect on cycling exercise performance. In conclusion, L-Arg infusion during exercise significantly increases skeletal muscle glucose clearance in humans. Because plasma insulin concentration was unaffected by L-Arg infusion, greater NO production may have been responsible for this effect.     

Glucagon increases insulin levels by stimulating insulin secretion without effect on insulin clearance in mice

Circulating insulin is dependent on a balance between insulin appearance through secretion and insulin clearance. However, to what extent changes in insulin clearance contribute to the increased insulin levels after glucagon administration is not known. This study therefore assessed and quantified any potential effect of glucagon on insulin kinetics in mice. Prehepatic insulin secretion in mice was first estimated following glucose (0.35 g/kg i.v.) and following glucose plus glucagon (10 μg/kg i.v.) using deconvolution of plasma C-peptide concentrations. Plasma concentrations of glucose, insulin, and glucagon were then measured simultaneously in individual mice following glucose alone or glucose plus glucagon (pre dose and at 1, 5, 10, 20 min post). Using the previously determined insulin secretion profiles and the insulin concentration-time measurements, a population modeling analysis was applied to estimate the one-compartment kinetics of insulin disposition with and without glucagon. Glucagon with glucose significantly enhanced prehepatic insulin secretion (Cmax and AUC_0-20) compared to that with glucose alone (p < 0.0001). From the modeling analysis, the population mean and between-animal SD of insulin clearance was 6.4 ± 0.34 mL/min for glucose alone and 5.8 ± 1.5 mL/min for glucagon plus glucose, with no significant effect of glucagon on mean insulin clearance. Therefore, we conclude that the enhancement of circulating insulin after glucagon administration is solely due to stimulated insulin secretion.     

Age-associated blood glucose levels during exercise in female swimmers

The purpose of this study was to determine whether age-associated alterations in blood glucose levels occur during exercise. In addition, blood lactate and fitness levels (VO2max) were examined to ascertain if these factors influenced the age-related responses. Sixty-four female masters swimmers (25-75 years) were classified into either a well trained (WT) or recreational trained (RT) group and exercised on a treadmill to VO2max X VO2max data confirmed our classification of WT and RT swimmers based on activity levels. There were no differences in post-absorptive blood glucose and lactate levels across age and fitness. Significant age-related effects on blood glucose levels during exercise (p less than 0.01) but no fitness effect were revealed by ANOVA. Within the first or second exercise stage all age groups demonstrated a significant decline in blood glucose (6.3 to 14.1%). A hyperglycemic response was observed during recovery in all age groups with the exception of the over 60 (60+) group. The 60+ group exhibited lower blood glucose levels compared to all other age groups during exercise commencing with the second exercise stage. There were no significant differences in glucose levels among any of the other age groups during exercise or recovery. There were no age-related differences in maximal or recovery lactates. These data indicate that there is an alteration of blood glucose homeostasis during exercise in females over 60 years of age.     

Influence of chalcone analogues on serum glucose levels in hyperglycemic rats

A series of chalcone derivatives from 3,4-methylenedioxybenzaldehyde and substituted acetophenones have been synthesized and investigated as antihyperglycemic agents in a glucose loaded animal model. Chalcones with biological activity were compared with lispro, regular insulin and tolbutamide effects on serum glucose levels. Compound 01, without substituent in the A-ring was not able to change glycemic levels. On the other hand, compounds 03, 04, 05, 09 and 10 with substitutions at position 3' and/or 4' in the A-ring caused significant reduction in serum glucose levels. Concerning the antihyperglycemic effect, compounds 03 and 05 (methoxy substituent) inhibited the hyperglycemia induced by glucose around 96% similar to that demonstrated for lispro insulin and tolbutamide at 60 min. A rapid and lasting antihyperglycemic effect was found with compound 09 and 10 (nitro substituent). In conclusion, besides the nature of the functional groups electron-donor substituent, as methoxy and hydroxyl or electron-acceptor, as nitro groups, the position of the group may be mandatory for biological activity.