Search PubMedSearch

PubMed · 1672241

Decrease in muscle glucose transporter number in chronic physical inactivity in rats.

Abstract

In this study, whole body insulin action on glucose uptake and muscle glucose transporter number of rats subjected to 14 days of physical inactivity conditions was examined. Unlike other suspension and denervation models of muscle disuse, this physical inactivity model allows voluntary contractile activity with minimal stress. Minimal depression of body weight gain and significant depression of gastrocnemius muscle growth were observed compared with that of control rats after 14 days of physical inactivity. The whole body insulin sensitivity and responsiveness were determined by the euglycemic clamp technique, with 1.4, 3.6, and 14 mU insulin.kg-1.min-1 perfusion and 2-deoxy-D-[3H]glucose incorporation. The rates of glucose disposal were the same in the restrained rats as in the controls with the 1.4 and 3.6 mU insulin perfusion; however, glucose disposal significantly decreased with 14 mU insulin perfusion. 2-Deoxy-D-[3H]glucose uptake into the gastrocnemius muscle was higher in the control rats than in the physically inactive rats. Glucose transporters in the gastrocnemius and quadriceps muscles, measured by means of the D-glucose-inhibitable cytochalasin B binding assay, were significantly decreased in number in the physically inactive rats. These findings suggest that the decrease in whole body glucose uptake might in part be explained by the decreases in the total glucose transporter number in muscles.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T Fushiki, T Kano, K Inoue, E Sugimoto. 1991. Decrease in muscle glucose transporter number in chronic physical inactivity in rats.. https://doi.org/10.1152/ajpendo.1991.260.3.e403

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Early glucocorticoid induction of calmodulin and its suppression by corticotropin-releasing factor in pituitary corticotrope tumor (AtT20) cells.

Glucocorticoids inhibit stimulus-evoked ACTH secretion by the rapid induction of new protein(s) that suppress intracellular free calcium signals. The present study examined whether the calcium receptor protein, calmodulin, is induced by glucocorticoids in the mouse pituitary corticotrope tumor (AtT20 D16:16) cell line. Treatment of AtT20 D16:16 cells with the synthetic glucocorticoid dexamethasone markedly (up to 10-fold) increased the level of a single (approximately 1.6kb) calmodulin mRNA 90 min after the application of steroid. Puromycin applied 15 min before and during dexamethasone treatment blocked the induction of this mRNA, suggesting that additional glucocorticoid induced transcription factor proteins may be required for enhanced calmodulin gene transcription. A two-fold increase in the intensity of an approximately 18K immunoreactive calmodulin protein band was detected by immunoblotting at 90 min after dexamethasone administration. Corticotropin releasing factor, added for 30 min at the start of steroid treatment, prevented the increase of calmodulin mRNA, as well as the suppression of corticotropin releasing factor-evoked ACTH release caused by dexamethasone. These data suggest that calmodulin may be involved in the early phase of glucocorticoid inhibition of pituitary ACTH release.

Adrenocorticotropic Hormone

ACTH: a structure-activity study on pilocarpine-induced epilepsy.

Intracerebroventricularly applied pilocarpine (2.4 mg/2 microliters) immediately produced symptoms of epilepsy, ranging from akinesia to motor seizures, in rats. Whereas ACTH-(1-39), ACTH-(1-24), ACTH-(1-18), ACTH-(1-16) and ACTH-(18-39) were not active, subcutaneous pretreatment with smaller ACTH-like fragments, such as ACTH-(4-9), ACTH-(4-10), ACTH-(4-10)(7D-Phe), ACTH-(7-16), and Org2766, reduced the severity of the epilepsy. Moreover, fewer rats developed motor seizures. Thus, ACTH fragments devoid of peripheral endocrine activity reduce pilocarpine-induced epileptiform activity in rats. A narrow bell-shaped dose-response relationship was found. Except for ACTH-(7-16), which was active in a dose of 1 and 10 micrograms/rat s.c., the other fragments were only active at one dose (10 micrograms/rat). The anti-epileptic properties appeared to reside in the sequence 1-16, and more specifically in the sequences 4-7 and 7-16, of the ACTH molecule.

Adrenocorticotropic Hormone

The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone.

Our previous studies have shown that stimulation of the anteroventral third ventricle region increases atrial natriuretic peptide (ANP) release, whereas lesions of the anteroventral third ventricle or median eminence block the release of ANP from blood volume expansion, suggesting a critical central nervous system participation in this response. ANP is also produced within neurons that have cell bodies in the rostral hypothalamus and axons that extend to the median eminence and neural lobe. In addition to its natriuretic effect, the peptide can inhibit the release of corticotropin (ACTH) and prolactin, anterior pituitary hormones that are released during stress. To determine the physiologic significance of ANP in the control of basal and stress-induced release of anterior pituitary hormones, highly specific antiserum against the peptide (AB-ANP) was microinjected into the third cerebral ventricle of conscious freely moving male rats to immunoneutralize hypothalamic ANP. In the initial experiment, the antiserum or control normal rabbit serum (NRS) was injected into the third cerebral ventricle to determine the effect of the antiserum on basal release of pituitary hormones. The antiserum had no effect on the concentrations of plasma ACTH, prolactin, or thyroid-stimulating hormone for 3 hr after the injection; however, plasma growth hormone concentration, although unchanged for 2 hr, was markedly elevated at 3 hr. These results indicate that although ANP appears to have no effect on the basal release of the other hormones, it has a physiologically significant inhibitory effect on growth hormone release. The delay of the effect is probably related to the time required for the antiserum to diffuse to the site of action of the peptide, presumably at some distance from the ventricle. Since this effect was demonstrable only after 3 hr, in the stress experiment, the antiserum or NRS was microinjected into the third ventricle 3 hr prior to application of ether stress. The rapid elevation of plasma ACTH in NRS-injected rats was markedly augmented by AB-ANP. Ether also induced a rapid increase in plasma prolactin in the NRS-injected animals, as expected. Contrary to the ACTH response, the maximal increase in plasma prolactin after ether was attenuated in animals preinjected with AB-ANP. In the NRS-injected animals, there was a significant decline in plasma growth hormone after the application of ether that was significantly accentuated by AB-ANP, but this was probably the result of the higher initial levels of plasma growth hormone in the ANP-AB group followed by its disappearance with a half-time similar to that of the NRS-injected group. The decline in plasma thyroid-stimulating hormone after ether stress was unaltered in the animals injected with AB-ANP. The results of these immunoneutralization studies suggest that endogenous ANP does not play a role in thyroid-stimulating hormone release. On the other hand, the endogenous peptide appears to have a physiologically significant inhibitory role in suppressing ACTH release during stress, mediated at least partly by suppression of vasopressin release. Endogenous ANP has a pathophysiologic role in augmenting the prolactin release in stress either by inhibiting release of prolactin-inhibiting factors or, alternatively, by enhancing release of prolactin-releasing factors. Endogenous ANP appears to inhibit resting, without altering stress-induced inhibition of growth hormone release by stimulating somatostatin release and/or inhibiting growth hormone-releasing hormone release or by both actions.

Adrenocorticotropic Hormone