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-dependent stress response involving DNA-PK occurs in hypoxic cells and contributes to cellular adaptation to hypoxia . Journal of Cell Science 124 1943 – 1951 . ( doi:10.1242/jcs.078030 ) Branco MR Oda M Reik W 2008 Safeguarding parental
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Laboratory of Intestinal Adaptation and Recovery, Departments of Pediatric Surgery B, Pathology, Section of Pediatric Surgery, The Ruth and Bruce Rappaport Faculty of Medicine, Technion‐Israel Institute of Technology, Haifa, Israel
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I Mogilner J Shamir R Shehadeh N Bejar J Hirsh M Coran AG 2005 Effect of subcutaneous insulin on intestinal adaptation in a rat model of short bowel syndrome . Pediatric Surgery International 21 132 – 137 . ( doi:10.1007/s00383
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Abstract
Phosphate (Pi) deprivation and IGFs stimulate renal Pi reabsorption. We studied the involvement of IGFs in the adaptation of Pi transport to Pi deprivation in MDCK cells.
Deprivation of Pi for 15 h increased the steady-state content of IGF-II mRNA (77 ± 12% whereas IGF-I mRNA was not detectable in MDCK cells in either control or Pi-deprived cells. IGF-II (10 −7 m) and IGF-I 10−8 m) stimulated the Na-dependent Pi uptake (1·23and 1·3-fold increase at 15 h respectively). The effect of IGF-I appeared after 15 h and increased up to 40 h of treatment (2·15-fold increase). In contrast, Pi uptake was increased by Pi deprivation as early as 8 h (1·5-fold) and up to 40 h of Pi deprivation (1·9-fold increase). IGF-II mRNA was not increased before 15 h of Pi deprivation and returned to control at 40 h. The combination of IGF-I and Pi deprivation had a more than additive effect on Pi transport (fivefold increase) (P<0·001).
At variance with Pi deprivation, high concentrations of insulin stimulated Na-coupled alanine transport (6 ± 2% and 16 ± 4% in Pi-treated and Pi-depleted cells respectively). Pi deprivation and high concentrations of insulin decreased Na,K-ATPase activity (−48 and −64% respectively) and these effects were not additive.
We concluded that: (1) long-term Pi deprivation increased the content of IGF-II mRNA in MDCK cells but that the paracrine/autocrine effects of IGFs could not account for the effects of Pi deprivation on Pi transport in MDCK cells and (2) IGFs could be involved in other changes occurring during Pi deprivation such as the decrease in Na,K-ATPase activity.
Journal of Endocrinology (1995) 145, 325–331
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Kloet ER Joëls M Holsboer F 2005 Stress and the brain: from adaptation to disease . Nature Reviews. Neuroscience 6 463 – 475 . Koletsky S Shook P Rivera-Velez J 1972 Absence of a hyperactive renal humoral pressor system in spontaneously
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The alterations in water homeostasis which accompany human pregnancy provide a unique example of resetting of osmolar control. The changes have inherent interest as a physiological adaptive mechanism, but do they have pathological significance for patients with previously unrecognized disturbance of water balance? In this commentary we highlight briefly the physiological changes in osmoregulation which occur in pregnancy. The possible mechanisms for these changes, including alterations in the metabolism and action of arginine vasopressin (AVP), are described and we attempt to relate these to the rare, but well recognized, phenomenon of exacerbation of subclinical diabetes insipidus in pregnancy. The tentative associations between AVP metabolism, pre-eclampsia and diabetes insipidus are also addressed.
Physiological water retention of pregnancy
Normal pregnancy is characterized by an early decrease in serum osmolality of up to 10 mosmol/kg which continues throughout gestation (Davison, Valloton & Lindheimer, 1981). This hypotonicity is maintained by a decreased osmotic threshold
IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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IGH/UPR, CNRS 1142, 141 rue de la Cardonille, 34396 Montpellier Cedex 05, France
Department of Animal Physiology, Faculty of Science, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands
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et al. 1987 , Manzon 2002 ) or growth hormone (i.e. the gh/igfI axis; Sakamoto et al. 1993 , McCormick 2001 ) in the adaptation to gradual or rapid salinity changes; also in the ontogenetic acquisition of salinity tolerance, these hormones play
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Parathyroid function was studied in 14 normal dogs 1 month before and after daily i.v. administration of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) (eight dogs), or about 50% parathyroidectomy (six dogs), to test the hypothesis that degradation of newly synthesized intact parathyroid hormone (I-PTH) is involved in parathyroid gland adjustment to a modified demand for I-PTH. Parathyroid function was studied through i.v. infusions of Na2EDTA and CaCl2 and measurement of ionized calcium (Ca2+), I-PTH and carboxyl-terminal PTH (C-PTH) at various time points. The C-PTH/I-PTH ratio was used as an index for change in the relative proportion of circulating C-PTH vs I-PTH, 1 month prior to and following each intervention. This ratio was further validated by looking at the HPLC profile of I- and C-PTH in hypo- and hypercalcemia under experimental conditions. Basal Ca2+ was unaltered 1 month after surgery, and was maintained constant in the 1,25-(OH)2D3-treated group by gradually decreasing 1,25-(OH)2D3 doses over time from 0.25 to 0.13 microgram twice daily during the last week of the experimental protocol. In this same group, basal 1,25-(OH)2D3 was increased by 65% (P < 0.0001) and basal I-PTH was decreased by 40% (P < 0.05), while basal C-PTH and the C-PTH/I-PTH ratio remained unchanged. Stimulated and non-suppressible I- and C-PTH followed the same pattern with, this time, an increase of stimulated and non-suppressible C-PTH/I-PTH ratio of 60% (P < 0.05) and 85% (P < 0.05) respectively. There was no change in basal I-PTH, C-PTH, or C-PTH/I-PTH ratio after surgery. However, stimulated I- and C-PTH were decreased by 45% (P < 0.005) and 65% (P < 0.005) respectively, with a 30% (P < 0.005) decrease of stimulated C-PTH/I-PTH ratio. There was no change in non-suppressible I-PTH, while non-suppressible C-PTH decreased by 55% (P < 0.005), with a 55% (P < 0.05) decrease in non-suppressible C-PTH/I-PTH ratio. The HPLC profiles of I- and C-PTH obtained in hypo- and hypercalcemia disclosed a similar distribution of the immuno-reactivity into peaks before and after i.v. administration of 1,25-(OH)2D3 as well as partial parathyroidectomy. This indicated that C-PTH/I-PTH ratio changes were related to different circulating levels of I- and C-PTH rather than to a different composition of I- and C-PTH. These data indicate a shift in the circulating PTH profile toward more PTH carboxyl-terminal fragments after 1 month of i.v. 1,25-(OH)2D3, but toward more intact PTH 1 month after about 50% parathyroidectomy, possibly reflecting adjustments in PTH degradation induced by a modified demand for I-PTH. Although these changes are most likely modulated at the parathyroid gland level, we cannot formally eliminate participation of the hormone's peripheral metabolism.
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Pregnancy is associated with adaptive changes including increased number and size of beta cells and enhanced gap-junctional coupling among beta cells, increased glucose-induced insulin response and decreased glucose stimulation threshold. The role exerted by pregnancy steroids and lactogenic hormones in the development of islets upregulation during pregnancy has been widely investigated. In the present study we studied the possibility that pregnancy steroids induce functional modifications of beta cells involving the expression and function of glucokinase. Our results indicate that estradiol and progesterone do not influence significantly glucokinase mRNA expression, while they induce a dose-dependent and time-dependent increase of glucokinase activity in RIN 1046-38 cells. The increased enzymatic activity results in an increased glucose-induced insulin release. Therefore it is possible to hypothesize that pregnancy steroids influence glucokinase expression in beta cells at a post-transcriptional level and that this effect contributes to the development of hyperinsulinemia during pregnancy.
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ABSTRACT
Specific binding sites for chum salmon growth hormone (sGH) were identified in the membranes obtained from tissues of rainbow trout. Specific binding of 125I-labelled sGH (% per mg protein) was found in the liver (37%), ovary (6%), brain (6%), gill (4%), intestine (4%) and posterior body kidney (4%). Specific binding was not significant in head kidney, anterior body kidney, spleen, heart, skeletal muscle or skin. Scatchard analyses demonstrated the presence of a single class of high-affinity low-capacity receptors in the liver, gill, intestine and kidney. The association constants for the membranes from liver, gill, intestine and kidney were of the same order (1 litre/nmol). Chum salmon prolactin did not inhibit the binding of 125I-labelled sGH to receptors in the liver, gill, intestine and kidney.
Transfer of rainbow trout from fresh water to 80% seawater evoked a rise in plasma concentration of GH and a significant decrease in the GH binding to the liver membranes after 1 day. Binding in the gill and kidney was not altered significantly. Membranes were treated with 4 mol MgCl2/l to remove bound GH from the receptors, and the results indicated that the reduction in binding in the liver after transfer to sea-water was probably due to receptor occupancy by increased endogenous GH. The occupancy of liver GH-binding sites was maximal 4 days after transfer. Total (MgCl2-treated) binding sites in the liver increased significantly 14 days after transfer. Scatchard analysis indicated that receptors were altered in capacity without changes in binding affinity. Although GH may also directly affect osmoregulatory organs through their GH receptors, the present results indicate the likelihood of at least partial mediation by the liver of the seawater-adapting action of GH in the rainbow trout.
Journal of Endocrinology (1991) 130, 425–433
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SUMMARY
When exposed to a low ambient temperature of 5 °C, adrenalectomized echidnas were able to increase their metabolic rate and to maintain their body temperature within the normal range for no more than 48 h — less than 12 h in five out of six animals. Thereafter, activity, metabolic rate, cardiac rate and body temperature declined and the animals became torpid.
When maintained with daily i.m. injections of 1–2 mg cortisol acetate/kg, adrenalectomized echidnas maintained activity and normal body temperature in the cold environment indefinitely. When cortisol injections were withheld and exposure to cold continued, normal body temperature was maintained for a further 10 days, after which it declined rapidly.
The onset of torpor was always preceded by a marked fall in plasma glucose concentration, as occurred in normal, but fasted, echidnas after prolonged exposure to cold. Both cortisol and corticosterone have glucocorticoid activity in echidnas, and torpor was prevented in adrenalectomized echidnas by preventing the fall in plasma glucose with either intermittent injections or constant rate infusions of glucose solutions.
The adrenal glands of normal echidnas exposed repeatedly to low environmental temperatures showed marked hypertrophy and increase in lipid content.
It is concluded that adrenocortical secretions are necessary for the metabolic response to cold stress in these prototherian mammals, and a major role of the corticosteroids is in maintenance of normal blood glucose concentrations, presumably by enhancing hepatic gluconeogenesis.
