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PubMed1999

Germination and growth responses of hybridizing Carpobrotus species (Aizoaceae) from coastal California to soil salinity.

Germination, growth, and physiological responses of hybridizing Carpobrotus from coastal California to soil salinity were studied. Hybrids are presumably the result of hybridization and introgression between the exotic Carpobrotus edulis, a succulent perennial invading coastal habitats, and the native or long-naturalized C. chilensis. Germination responses were investigated at 0, 10, 20, and 50% seawater. Seedling growth and physiology were compared by irrigating seedlings with solutions of the same seawater concentrations and in low and high nutrients. Germination was inhibited in the presence of salt, but recovered after transferring the seeds to fresh water. Seeds exposed to salt had higher final germination rates than control. Growth of Carpobrotus was slightly enhanced by low seawater concentrations but reduced at high salinity at both nutrient regimes. Leaf cell sap osmolarity increased with increasing soil salinity, and taxa did not differ significantly in this physiological adjustment. Leaf carbon isotope ratios (∂(13)C) ranged from -28 to -22‰ and became less negative at higher salinities, indicating an improved water use efficiency in the seedlings at high salt concentrations. In addition, ∂(13)C values were generally less negative at high than at low nutrients. Differences among taxa were generally small. The results show that salinity affects both establishment and growth of hybridizing Carpobrotus. The overall weak species differences in salt tolerance indicate that the exotic C. edulis can occupy the same sites as C. chilensis in terms of salinity. The similarity of hybrids in their response to salinity suggests that they may contribute to the invasion by Carpobrotus.

Journal Article↗
PubMed1998

Osmotic effects as a factor modifying insecticide toxicity on Aedes and Artemia.

Euryhaline species are more tolerant of various insecticides under isosmotic conditions. Two euryhaline species, Aedes taeniorhynchus (Wiedemann) and Artemia sp., were exposed to four insecticides (aldicarb, dimethoate, imidacloprid, tebufenozide), under isosmotic and hyperosmotic conditions. Mortality under these two osmotic conditions was observed and compared to evaluate salinity as a contributing factor to insecticide toxicity. Artemia was more tolerant of all chemicals tested than A. taeniorhynchus under isosmotic conditions based on the percentage mortality observed. Mortality of Artemia under isosmotic conditions was dependent on the length of exposure; A. taeniorhynchus did not exhibit time dependence. Less mortality was observed in populations of both test species under isosmotic conditions compared with hyperosmotic conditions. However, the variation in mortality due to exposure to test chemicals was of greater magnitude in A. taeniorhynchus than Artemia. This result indicates that higher salinity is a greater stress on A. taeniorhynchus than Artemia when exposed to the test insecticides at the concentration ranges tested in this study.

Aedes↗
PubMed2004

Adenoviral-mediated transfer of vascular endothelial growth factor 121 cDNA enhances myocardial perfusion and exercise performance in the nonischemic state.

BACKGROUND: Angiogenic gene therapy has been demonstrated to enhance perfusion to ischemic tissues, but it is unknown whether the administration of angiogenic growth factors will increase blood flow to nonischemic tissues. This study investigates whether enhanced myocardial perfusion can be mediated by adenovirus-mediated transfer of vascular endothelial growth factor 121 cDNA to nonischemic myocardium. METHODS: New Zealand White rabbits received adenovirus (5 x 10(10) particle units) encoding for vascular endothelial growth factor 121 (n = 14) or a control vector without a transgene (n = 13) or saline solution (n = 9) via direct myocardial injection. Fluorescent microsphere perfusion studies and histologic analyses were performed 4 weeks later. In a parallel study, exercise treadmill testing was performed to assess the functional effects of this therapy in Sprague-Dawley rats. RESULTS: Microsphere assessment of myocardial perfusion in rabbits 4 weeks after adenovirus-encoding vascular endothelial growth factor administration was greater than that for rats injected with control vector without a transgene or saline solution (3.2 +/- 0.5 vs 2.7 +/- 0.7 and 2.4 +/- 0.4, respectively; P <.03). The endothelial cell count per high power field was increased in animals injected with adenovirus-encoding vascular endothelial growth factor versus animals injected with control vector without a transgene or saline solution (147 +/- 27 vs 123 +/- 14 and 125 +/- 16 cells, respectively), although this did not reach statistical significance (P =.12). Rats treated with adenovirus-encoding vascular endothelial growth factor also demonstrated prolonged exercise tolerance compared with rats injected with control vector without a transgene or saline solution (exhaustion time: 26 +/- 5 minutes vs 19 +/- 2 minutes and 20 +/- 3 minutes, respectively; P =.006). CONCLUSIONS: Adenovirus encoding-mediated transfer of vascular endothelial growth factor 121 induces an enhancement in regional perfusion in nonischemic myocardium that corresponds to changes in exercise tolerance. Adenovirus-encoding vascular endothelial growth factor therapy may be useful for inducing angiogenesis in the nonischemic state, such as for prophylactic therapy of early coronary artery disease.

Adenoviridae↗
PubMed2006

Aster tripolium L. and Sesuvium portulacastrum L.: two halophytes, two strategies to survive in saline habitats.

Aster tripolium L. (Dollart, Germany) and Sesuvium portulacastrum L. (Dakhla, Morocco) are potential halophytic vegetables, fodder plants, and ornamentals for re-vegetating saline land. To compare their strategies involved in salt tolerance both plants were grown with 0%, 1.5%, and 3% (Aster) or 0%, 2.5%, and 5% (Sesuvium) NaCl in the watering solution. The growth rate was reduced in both species with increasing NaCl concentrations. The quotient of Na(+)/K(+) indicates that Aster accumulates more K(+) in comparison to Na(+) while the reverse is true for Sesuvium. Osmolality of the leaf sap increased with increasing NaCl concentration in both Aster and Sesuvium. Transpiration rate was severely reduced in both Aster (3%) and Sesuvium (5%) plants after 10 d of NaCl watering. The CO(2) assimilation rate decreased in Aster (3%) and Sesuvium (5%) NaCl-treated plants from day 5 to day 10. The most important results from chlorophyll fluorescence measurements were derived from the non-photochemical quenching analysis (NPQ). First, both plants had linearly increasing levels of NPQ with increasing NaCl concentrations. Second, Sesuvium had almost half the NPQ value when compared to Aster under increased soil salinity. In Aster P-ATPase activities were decreased in plants treated with 3% NaCl after three days of treatment, F-ATPase activities increased with increasing NaCl concentrations and no clear changes were measured in V-ATPase activities. In Sesuvium any changes could be observed in the three ATPase activities determined. To conclude, Aster and Sesuvium use different strategies in adaptation to soil salinity.

Adenosine Triphosphatases↗
PubMed2002

Important roles of drought- and cold-inducible genes for galactinol synthase in stress tolerance in Arabidopsis thaliana.

Raffinose family oligosaccharides (RFO) accumulating during seed development are thought to play a role in the desiccation tolerance of seeds. However, the functions of RFO in desiccation tolerance have not been elucidated. Here we examine the functions of RFO in Arabidopsis thaliana plants under drought- and cold-stress conditions, based on the analyses of function and expression of genes involved in RFO biosynthesis. Sugar analysis showed that drought-, high salinity- and cold-treated Arabidopsis plants accumulate a large amount of raffinose and galactinol, but not stachyose. Raffinose and galactinol were not detected in unstressed plants. This suggests that raffinose and galactinol are involved in tolerance to drought, high salinity and cold stresses. Galactinol synthase (GolS) catalyses the first step in the biosynthesis of RFO from UDP-galactose. We identified three stress-responsive GolS genes (AtGolS1, 2 and 3) among seven Arabidopsis GolS genes. AtGolS1 and 2 were induced by drought and high-salinity stresses, but not by cold stress. By contrast, AtGolS3 was induced by cold stress but not by drought or salt stress. All the GST fusion proteins of GST-AtGolS1, 2 and 3 expressed in Escherichia coli had galactinol synthase activities. Overexpression of AtGolS2 in transgenic Arabidopsis caused an increase in endogenous galactinol and raffinose, and showed reduced transpiration from leaves to improve drought tolerance. These results show that stress-inducible galactinol synthase plays a key role in the accumulation of galactinol and raffinose under abiotic stress conditions, and that galactinol and raffinose may function as osmoprotectants in drought-stress tolerance of plants.

Acclimatization↗
PubMed2006

Behavioral and electrophysiological evidence for opioid tolerance in adolescent rats.

Morphine and other opiates are successful treatments for pain, but their usefulness is limited by the development of tolerance. Given that recent studies have observed differential sensitivity to drugs of abuse in adolescents, the aim of this study was to assess antinociceptive tolerance to morphine in adolescent rats using both behavioral and cellular measures. Early (28-35 days postnatal) and late (50-59 days) adolescent and adult (73-75 days) male rats were injected with morphine (5 mg/kg, s.c.) or saline twice a day for two consecutive days. On Day 3, tolerance to morphine was evident in morphine-pretreated rats when tested on the hot plate test. Although baseline latencies for the early compared to late adolescent rats were faster, the magnitude of the shift in ED(50) for morphine was similar for the two adolescent groups. However, the shift in ED(50) tended to be greater in adolescent compared to adult rats. Subsequent to behavioral testing, whole cell patch-clamp recordings were made from ventrolateral PAG neurons. The opioid agonist, met-enkephalin (ME), activated similar outward currents in PAG neurons of early and late adolescent rats. However, reversal potentials of ME-induced currents were shifted to more hyperpolarized potentials in cells from morphine-pretreated rats. In addition, ME induced larger currents in morphine-pretreated rats with faster hot plate latencies compared to the mean (more tolerant) than in rats with slower latencies. These results indicate that repeated intermittent administration of morphine produces tolerance in adolescent rats that is associated with novel changes in opioid-sensitive ventrolateral PAG neurons.

Action Potentials↗
PubMed1987

Genetic influences on tolerance development with chronic oxotremorine infusion.

Mice of four inbred strains (BALB, C57BL, DBA and C3H) were administered either saline or oxotremorine, a muscarinic agonist, at a dose of 0.5 mg/kg/hr by constant infusion through cannulas implanted in the right jugular veins. Chronic treatment resulted in the development of tolerance to the effects of oxotremorine both on rotarod performance and on body temperature. For drug-treated BALB mice, the dose-response curves for both measures were parallel to those for saline-treated mice, while for DBA and C3H mice the slopes of the dose-response curves were significantly less for treated mice than they were for controls. The equi-effective doses for the drug-treated animals were at least 8-fold greater than those for saline-treated mice. Drug treatment resulted in a significant decrease in the total number of muscarinic receptors in cortex as measured by the binding of [3H]quinuclidinyl benzilate (QNB) without effect on the KD for this ligand. Similarly, drug treatment did not affect the affinity of carbamylcholine as an inhibitor of QNB binding, but did significantly decrease the levels of both the high- and low-affinity agonist binding sites in cortex. The number of M1 muscarinic receptors measured by high affinity [3H]pirenzepine (PZ) binding was also significantly decreased in cortex without effect on the KD. The experiments were extended to five other brain regions. Full saturation curves were not constructed, however. Oxotremorine treatment significantly reduced QNB binding in every brain region. While the binding to agonist affinity states measured by carbamylcholine inhibition of QNB binding and M1 receptor levels measured by high affinity PZ binding tended to decrease with oxotremorine treatment not all changes were statistically significant. The changes in muscarinic receptor subtype levels induced by oxotremorine infusion did not differ among the strains. The results demonstrate that chronic treatment with a muscarinic agonist results in substantial tolerance to the effects of the drug in all four mouse strains. Although some differences in tolerance development exist, these differences are not readily explained by differences in the number or affinity states of brain muscarinic receptors.

Animals↗
PubMed1978

[Improvement of pathological glucose tolerance by bradykinin in diabetics and in surgical patients (author's transl)].

Intravenous glucose tolerance tests (GTT) were performed in 13 metabolically healthy patients at the first and second day after abdominal surgery. GTT were carried out during an additional infusion of bradykinin (BK) (80 microgram/h) in six of these patients at the first day (group A) and in seven patients at the second day (group B). Furthermore, GTT were performed in six patients with chemical diabetes with and without BK-infusion. In addition, the effect of BK on blood glucose concentration in the postabsorptive state was investigated in nine maturity onset diabetics and in five healthy volunteers. As a control, another nine diabetics received physiological saline. In both groups of surgical patients BK improved glucose tolerance (k-values: group A without BK 1.03 +/- 0.12, with BK 1.31 +/- 0.07; group B without BK 0.85 +/- 0.18, with BK 1.25 +/- 0.21). This was also true in chemical diabetics (without BK 0.81 +/- 0.03, with BK 1.08 +/- 0.04). While BK did not change blood glucose concentration in healthy volunteers, it reduced that of diabetics by 12.2 +/- 1.4% continuously during 100 min. No spontaneous drop of blood glucose was observed in diabetics receiving saline. These results are in good accord with the present view that kinins may play a role within the regulation of carbohydrate metabolism.

Blood Glucose↗
PubMed1999

The stimulation of low-affinity, nontolerized clones by heteroclitic antigen analogues causes the breaking of tolerance established to an immunodominant T cell epitope.

H-2K mice injected, intravenously in saline or intraperitoneally in incomplete Freund's adjuvant, with large quantities of the immunodominant I-E(k)-restricted epitope from moth cytochrome c (MCC) 88-103 fail to respond to subsequent immunization with this epitope when administered in complete Freund's adjuvant. This state of tolerance can be broken by immunization with certain MCC 88-103 analogues that are heteroclitic antigens as assessed on representative MCC 88-103 specific T cell clones. In this paper, the mechanism of breaking tolerance by heteroclitic antigens was investigated. The following observations were made: (a) T cell hybridomas derived from tolerance-broken animals required higher concentrations of MCC 88-103 to be stimulated than hybridomas derived from normal immune animals, suggesting that they have T cell receptors (TCRs) of lower affinity; (b) in contrast to normal immune animals whose MCC-specific TCRs are typically Vbeta3(+)/Valpha11(+), none of the hybridomas derived from tolerance-broken animals expressed Vbeta3, although they were all Valpha11(+). Also, the Vbeta complementarity determining region 3 (CDR3) regions from the tolerance-broken animals did not contain the canonical structure and length characteristics of the normal MCC 88-103 immune repertoire; and (c) adoptive transfer and tolerization of MCC-specific Vbeta3(+)/Valpha11(+) transgenic T cells followed by immunization with heteroclitic antigen failed to terminate the state of tolerance. Collectively, these data strongly suggest that the mechanism involved in breaking tolerance in this system is the stimulation of nontolerized, low-affinity clones, rather than reversal of anergy. Further support for this mechanism was the finding that after activation, T cells apparently have a lowered threshold with respect to the affinity of interaction with antigen required for stimulation.

Amino Acid Sequence↗
PubMed1989

Procedures that produce context-specific tolerance to morphine in rats also produce context-specific withdrawal.

Rats previously injected with morphine in the presence of a distinct environment (paired animals) were more tolerant to the analgesic effects of morphine in that environment than were rats previously injected with morphine in another environment (unpaired animals). When injected with saline instead of morphine in the distinct environment, paired animals were more reactive to pain (hyperalgesic) than unpaired animals, but no more reactive to pain than animals never given morphine. More important, the paired animals also exhibited more withdrawal symptoms (wet dog shakes, genital licking, circling, rearing, and defecation) during abstinence and naltrexone-precipitated withdrawal in the distinct environment than did the unpaired and saline animals. Thus, procedures that are capable of producing context-specific opiate tolerance are also capable of producing context-specific opiate withdrawal.

Animals↗
PubMed1971

The effect of administration of human growth hormone on the plasma growth hormone, cortisol, glucose, and free fatty acid response to insulin: evidence for growth hormone autoregulation in man.

The effect of administration of human growth hormone (HGH) (3 mg every 6 hr for 6 days) on the endogenous GH response to insulin-induced hypoglycemia at 8, 12, 24, and 48 hr posttreatment was studied in 11 healthy male adults. Free fatty acid, cortisol, and glucose responses pre- and posttreatment with HGH were evaluated concurrently. Control subjects received saline injections to evaluate relationship of GH responses to the periodicity of insulin tolerance tests. The data were compared for each subject pre- and posttreatment with HGH as well as by comparison of the results of the saline-treated group with those of the HGH-treated group. The mean maximal GH concentration in response to insulin-induced hypoglycemia for all the subjects (n = 16) was 31.1 +/-3.6 ng/ml (+/-SEM) on day 1 of the control period and 23.4 +/-3.1 (SEM) on day 2, not statistically significant.A significant decrease in the maximal peak GH response (n = 8) after insulin-induced hypoglycemia was observed at 8 and 12 hr after HGH administration was terminated with mean peak values for GH of 4.6 +/-1.3 ng/ml and 10.4 +/-1.9 ng/ml, respectively (P < 0.01). A progressive return to control values was noted between 12 and 24 hr. The GH responsiveness of the saline-treated group (n = 5) was unchanged from that observed during the control period. The fasting glucose values were unchanged in the GH-treated group from those of the control period or of the saline-treated controls. Insulin resistance was apparent at 8 hr posttreatment with HGH. No differences in FFA response after insulin-induced hypoglycemia were observed in GH-treated or saline-treated subjects. The rise in plasma cortisol after insulin-induced hypoglycemia was comparable in the GH-treated and saline-treated group. Diurnal variation in plasma cortisol was maintained during the period of GH suppression. These observations support the concept that GH can modulate its secretion by means of an auto-feedback mechanism.

Adult↗
PubMed1996

Effect of sensitization of stereotypy on the acquisition and retention of tolerance to amphetamine hypophagia.

The purpose of this study was to determine whether prior sensitization of stereotypy interferes with the development and retention of tolerance to amphetamine-induced hypophagia. Rats were given intermittent injections of either amphetamine (2.5 mg/kg) to induce sensitization of stereotypy, or saline. Subgroups from each group then received daily injections of either amphetamine (2 mg/kg) or saline and access to milk for 30 min. Both sensitized and nonsensitized groups became tolerant to drug-induced hypophagia at about the same rate and to about the same extent. Such tolerance was accompanied by a decrease in the frequency of stereotyped movements while milk was available. The rats were then given daily milk tests for 4 weeks without injections. Subsequent tests with amphetamine revealed that both groups lost tolerance to drug-induced hypophagia and displayed more intense stereotypy than they had prior to drug withdrawal. We conclude that sensitization of stereotypy produced by intermittent injections of amphetamine (2.5 mg/kg) does not retard the development of tolerance to drug-induced hypophagia and does not alter the rat's ability to suppress stereotyped movements. However, the loss of tolerance following drug withdrawal may have been due to the development of more intense stereotypy and/or the "unlearning" of previously acquired strategies for suppressing stereotypy.

Amphetamine↗
PubMed1991

Bromocriptine inhibits the seasonally occurring obesity, hyperinsulinemia, insulin resistance, and impaired glucose tolerance in the Syrian hamster, Mesocricetus auratus.

Seasonally obese-hyperinsulinemic female Syrian hamsters were injected daily with bromocriptine or saline for a period of 34 days to test for effects of bromocriptine on body fat store levels, hepatic triglyceride secretion, glucose tolerance, and plasma insulin and glucose concentrations. The effects of bromocriptine on body fat store levels, as well as on plasma insulin and glucose concentrations, in seasonally obese hamsters were compared with the levels of body fat, plasma insulin, and plasma glucose observed in seasonally lean hamsters. Bromocriptine treatment substantially improved glucose intolerance and reduced the total and stimulated areas under the glucose tolerance curve by 33% after 14 days of treatment. After 34 days of treatment, bromocriptine reduced body fat store levels by 36% and hepatic triglyceride secretion by 40% without any concurrent change in food consumption. Furthermore, bromocriptine reduced the plasma insulin level by 70%, while slightly reducing plasma glucose concentration (ie, 68% reduction in the insulin to glucose ratio). The reductions of body fat, plasma insulin, and plasma insulin to glucose ratio produced by bromocriptine in seasonally obese hamsters are equivalent to those observed in seasonally lean hamsters. Shifts in phase relationships of circadian neuroendocrine rhythms have been demonstrated to regulate annual cycles of metabolism in vertebrates, including the Syrian hamster. The effects of bromocriptine can also be explained as an alteration of such a circadian mechanism.

Adipose Tissue↗
PubMed1996

Unsignaled morphine delivery does not disrupt the development of associative morphine tolerance in the rat.

When morphine administration is paired with a distinctive context, tolerance to morphine's analgesic effects comes readily under the associative control of the drug-paired context. These associative tolerance effects are eliminated when a relatively short (i.e., 6 h) interdose interval (IDI) is used for conditioning. Contemporary models of learned tolerance explain the absence of learning at short IDIs by positing that residual morphine effects from a recent drug exposure disrupt the formation of drug-context associations. The present studies examined the impact of unsignaled morphine injections given 6 h prior to drug-context pairings on the development of associative tolerance. Analgesia was measured by the tail-flick method, and tolerance levels were assessed by dose-response curve methodology. Morphine preexposure had no detectable influence on the acquisition of associative tolerance when rats were tested immediately after conditioning, after a 30-day rest interval, or after a 30-day period of daily saline injections in their home-cage environment. These data suggest disruption of associative tolerance effects at short IDIs is not attributable to residual effects of morphine from the immediately preceding trial.

Animals↗
PubMed1999

Lack of cross-tolerance between the antinociceptive effects of systemic morphine and asimadoline, a peripherally-selective kappa-opioid agonist, in CCI-neuropathic rats.

The development of tolerance following repeated doses of morphine hinders the treatment of clinical pain. We have previously shown that morphine tolerance develops in neuropathic rats without cross-tolerance to a systemic kappa-opioid agonist; in the current work, using paw-pressure vocalization thresholds, we studied the antinociceptive effect of the peripherally-selective kappa (kappa)-opioid agonist, asimadoline, in both morphine-tolerant and opioid-naïve rats 2 weeks after sciatic nerve injury. In naïve rats, intraplantar (i.pl.) injection of asimadoline into the nerve-injured paw, at doses of 10, 15 and 20 (but not 30) microg, dose-dependently relieved the mechanical allodynia-like behaviour. The kappa-opioid antagonist, norbinaltorphimine, (30 microg, i.pl.) reversed this action; injection of asimadoline (15 microg) into the contralateral paw (i.pl.) or i.v., however, had no effect. These results confirm that at low doses, asimadoline exerts its action only in the periphery. In morphine-tolerant rats (after 10 mg/kg s.c. , twice daily for 4 days) and naïve, saline-pretreated rats, asimadoline (15 microg, i.pl.) relieved the mechanical allodynia-like behaviour to the same extent, indicating no cross-tolerance between morphine and the peripherally-selective drug. Our findings show promise for the treatment of neuropathic pain with low doses of peripherally-selective kappa-opioids.

Acetamides↗
PubMed1996

An antisense oligodeoxynucleotide to the delta opioid receptor (DOR-1) inhibits morphine tolerance and acute dependence in mice.

Pharmacological data from several laboratories support a modulatory role for the delta opioid receptor in morphine analgesia, tolerance, and physical dependence. We examined the role of the delta opioid receptor in these processes using an in vivo antisense strategy in mice. Intracerebroventricular administration of a 20mer antisense or a mismatch control oligodeoxynucleotide (ODN) targeting the mRNA of the cloned delta opioid receptor (DOR-1) for 3 days did not affect baseline nociceptive thresholds or morphine analgesia compared to untreated or saline-treated mice. However, dose-response studies indicate that the induction of morphine tolerance following 3 days of chronic morphine administration was blocked in antisense but not mismatch ODN or saline-treated mice. Antisense ODN treatment also blocked the development of acute morphine dependence, whereas similar protection was not afforded to mice treated with saline or mismatch ODN. This study demonstrates the relevance of the cloned DOR-1 in morphine tolerance and dependence and provides new evidence for a modulatory role of the delta opioid receptor using this novel approach.

Animals↗
PubMed2002

The absence of acute tolerance during remifentanil infusion in volunteers.

UNLABELLED: The development of acute opioid tolerance in humans remains controversial. We tested the hypothesis that continuous remifentanil infusion leads to rapid development of opioid tolerance. Twenty healthy male volunteers were enrolled onto a randomized, placebo-controlled, double-blinded, cross-over design study to receive a 3 h continuous infusion of remifentanil (0.08 microg x kg(-1) x min(-1)) or saline. Test procedures included determination of pain perception thresholds and pain tolerance thresholds to heat and cold and neuroselective sine wave constant current at 5 Hz and 250 Hz. Test procedures were performed at baseline and then repeated at 25, 55, 85, 115, and 160 min (heat/cold) and at 35, 65, 95, 125, and 170 min (electrical current) during infusion. No significant decrease of the pain threshold devolutions between 55 and 180 min after the start of infusion of remifentanil could be detected. In conclusion, no development of acute opioid tolerance was observed during constant remifentanil infusion of 3 h in volunteers. IMPLICATIONS: The opioid remifentanil was applied to 20 volunteers at a constant concentration for 3 h while pain thresholds to temperature and current were repeatedly assessed. Our aim was to study whether thresholds decrease over time because of the rapid development of opioid tolerance. No development of rapid opioid tolerance was observed.

Adult↗
PubMed2006

Calorie restriction initiated at middle age improved glucose tolerance without affecting age-related impairments of insulin signaling in rat skeletal muscle.

Calorie restriction (CR) may affect glucose tolerance via modulation of the insulin action in skeletal muscle. The present study investigated the effect of CR initiated at middle age in rats bearing glucose intolerance, in comparison with CR at a younger age. Male F344 rats at 2.5 and 18months (mo) of age were fed ad libitum (AL) or 30% CR diets for 4-4.5mo, subjected to glucose tolerance testing, and then sacrificed 15min after intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules. The protein abundance of phosphorylated (p) insulin receptors, p-Akt, and p-atypical PKC and the membrane fraction of glucose transporter 4 in quadriceps femoris muscle (QFM) were analyzed by EIA or immunoblotting. CR initiated either at young or middle age improved glucose tolerance with a lower serum insulin response to glucose. However, middle-aged CR did not improve aging-related impairments in insulin signaling in QFM. The present results emphasized the possibilities of CR activation of an insulin-independent mechanism in skeletal muscle and also of the involvement of non-muscle tissues in glucose uptake.

Adipose Tissue↗