Search Results
School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, Arizona, USA
Search for other papers by Xiaochuan Chen in
Google Scholar
PubMed
Search for other papers by Amy C Kelly in
Google Scholar
PubMed
Search for other papers by Dustin T Yates in
Google Scholar
PubMed
Search for other papers by Antoni R Macko in
Google Scholar
PubMed
Search for other papers by Ronald M Lynch in
Google Scholar
PubMed
Search for other papers by Sean W Limesand in
Google Scholar
PubMed
these two distinct models of chronic hypercatecholaminemia, PI-IUGR and NE infusion indicate that sustained adrenergic stimulation produces a compensatory augmentation in β-cell responsiveness. Therefore, we propose that NE-induced adaptations in fetal
Search for other papers by Liselotte Fransson in
Google Scholar
PubMed
Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden
Search for other papers by Stephanie Franzén in
Google Scholar
PubMed
Search for other papers by Victoria Rosengren in
Google Scholar
PubMed
Search for other papers by Petra Wolbert in
Google Scholar
PubMed
Department of Clinical Science and Education, Division of Drug Research, Center of Medical Image Science and Visualization, Department of Biochemistry and Molecular Biology, Södersjukhuset, Karolinska Institutet, SE-118 83 Stockholm, Sweden
Search for other papers by Åke Sjöholm in
Google Scholar
PubMed
Search for other papers by Henrik Ortsäter in
Google Scholar
PubMed
conclude that the increased demand on insulin secretion from the pancreatic islets, in this model with hyperglycemia and insulin resistance, is followed by an adaptation – not only via an increase in the number of β-cells and thus islet size – but also via
Search for other papers by Malathi Srinivasan in
Google Scholar
PubMed
Search for other papers by Paul Mitrani in
Google Scholar
PubMed
Search for other papers by Gigani Sadhanandan in
Google Scholar
PubMed
Search for other papers by Catherine Dodds in
Google Scholar
PubMed
Search for other papers by Suhad Shbeir-ElDika in
Google Scholar
PubMed
Search for other papers by Shanthie Thamotharan in
Google Scholar
PubMed
Search for other papers by Hussam Ghanim in
Google Scholar
PubMed
Department of Biochemistry, Department of Pediatrics, Department of Medicine, Diabetes and Endocrinology Center of Western New York, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York at Buffalo, 140 Farber Hall, 3435 Main Street, Buffalo, New York 14214, USA
Search for other papers by Paresh Dandona in
Google Scholar
PubMed
Search for other papers by Sherin U Devaskar in
Google Scholar
PubMed
Search for other papers by Mulchand S Patel in
Google Scholar
PubMed
isocaloric and isonitrogenous milk formula ( Patel & Srinivasan 2002 , Srinivasan et al . 2003 ). The immediate onset of hyperinsulinemia in the HC pups correlates with several adaptations in pancreatic β cells including the autonomic regulation of insulin
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Toshihiro Sugiyama in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Toshiaki Takaki in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Kenya Sakanaka in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Hiroki Sadamaru in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Koji Mori in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Yoshihiko Kato in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Toshihiko Taguchi in
Google Scholar
PubMed
Applied Medical Engineering Science, Graduate School of Medicine, Yamaguchi University, 2-16-1 Tokiwadai, Yamaguchi 755-8611, Japan
Search for other papers by Takashi Saito in
Google Scholar
PubMed
mineral formation de novo ( Hunter et al. 1996 ) and mice lacking osteopontin have larger mineral size ( Boskey et al. 2002 ) and stiffer bone tissue ( Duvall et al. 2007 ). Compensatory adaptation of warfarin
Search for other papers by I. G. WHITE in
Google Scholar
PubMed
1. The effect of twice-daily injections of formalin, as an agent eliciting the adaptation syndrome, has been studied on the blood constituents of sheep.
2. Within 4 days of the start of injections of 5 ml. of 4 % formalin there was a significant hypochloraemia, hypoglycaemia and leucocytosis with a return to normal levels after 10 days. There was also an intermediate compensatory hyperglycaemia. The leucocytosis was due primarily to a neutrophilia, although there was a slight transient increase in both absolute lymphocyte and eosinophil counts.
3. When the dose rate was increased to 10–20 ml. of 10% formalin, the plasma chloride and leucocyte patterns were repeated and there was also an increase in erythrocytes and haemoglobin values. In the later stages of the experiment the absolute lymphocyte and eosinophil counts were depressed, whilst the absolute monocyte count had risen.
4. There were no significant changes in blood acetone or in the basophil count throughout the experiment.
5. It is concluded that, in general, the blood changes elicited by an alarming stimulus in sheep are similar to those described in small laboratory animals. The renewed response to an increased intensity of stimulus observed in this experiment indicates that resistance is quantitatively as well as qualitatively specific.
Search for other papers by T Clark Brelje in
Google Scholar
PubMed
Search for other papers by Nicholas V Bhagroo in
Google Scholar
PubMed
Search for other papers by Laurence E Stout in
Google Scholar
PubMed
Search for other papers by Robert L Sorenson in
Google Scholar
PubMed
lipids induces a further adaptation in the islets. By late pregnancy, insulin secretion is less sensitive to glucose stimulation and becomes more dependent on the presence of fatty acids. This situation allows the maintenance of elevated insulin secretion
Search for other papers by R. G. BARTLETT Jr. in
Google Scholar
PubMed
Search for other papers by M. A. MILLER in
Google Scholar
PubMed
SUMMARY
The role of the adrenal cortex in restraint-induced hypothermia and in adaptation to the stress of restraint was investigated.
There was an increase in ascorbic acid and a less marked increase in the cholesterol content of the adrenals accompanying 1 week's exposure to the stress of light restraint to produce adaptation, as well as a decrease in the adrenal ascorbic acid and cholesterol levels accompanying restraintinduced hypothermia, but changes in adrenocortical activity were probably not of sufficient magnitude to account for either the increased thermostability after the adaptive procedure or the thermolability of the animals exposed to the short-term stress.
It was also demonstrated that after a 7-day exposure to light restraint (to produce adaptation), adrenalectomized animals, maintained with isotonic salt solution or DCA, could not maintain a normal body temperature when restrained in the cold. Cortisone, whether administered alone or with DCA, permitted these adrenalectomized, adapted animals to maintain essentially normal body temperatures when exposed to restraint in the cold, indicating that adaptation had occurred.
Search for other papers by Gustavo Canul-Medina in
Google Scholar
PubMed
Search for other papers by Leticia Riverón-Negrete in
Google Scholar
PubMed
Search for other papers by Karina Pastén-Hidalgo in
Google Scholar
PubMed
Search for other papers by Paulina Morales-Castillo in
Google Scholar
PubMed
Search for other papers by Francisco García-Vázquez in
Google Scholar
PubMed
Search for other papers by Cristina Fernandez-Mejia in
Google Scholar
PubMed
the endocrine pancreas for the adaptations that occur post-lactation. This condition resembles the increase in beta-cell replication and beta-cell hypertrophy that occur during two–thirds of the gestation period, anteceding the metabolic and islet mass
Search for other papers by Gabriel F Anhê in
Google Scholar
PubMed
Search for other papers by Tatiane C A Nogueira in
Google Scholar
PubMed
Search for other papers by José E Nicoletti-Carvalho in
Google Scholar
PubMed
Search for other papers by Camilo Lellis-Santos in
Google Scholar
PubMed
Search for other papers by Helena C Barbosa in
Google Scholar
PubMed
Search for other papers by José Cipolla-Neto in
Google Scholar
PubMed
Search for other papers by José R Bosqueiro in
Google Scholar
PubMed
Search for other papers by Antonio C Boschero in
Google Scholar
PubMed
Search for other papers by Silvana Bordin in
Google Scholar
PubMed
Introduction In pancreatic β-cells, the most prominent effect attributed to Janus kinase/signal transducer and activator of transcription 5 (JAK/STAT5) signaling pathway is the functional adaptation induced by placental lactogens (PL
Search for other papers by I Avril in
Google Scholar
PubMed
Search for other papers by B Blondeau in
Google Scholar
PubMed
Search for other papers by B Duchene in
Google Scholar
PubMed
Search for other papers by P Czernichow in
Google Scholar
PubMed
Search for other papers by B Breant in
Google Scholar
PubMed
We investigated the cellular mechanisms responsible for the inability of 8-month-old previously malnourished (PM) females to adapt their beta-cell mass during pregnancy. The evolution during pregnancy of beta-cell fraction, size and proliferation was studied. At day 21 of pregnancy beta-cell fraction increased less in PM than in control females, compared with their non-pregnant values. A slight beta-cell hypertrophy was observed during pregnancy in both groups. In control females, beta-cell 5-bromo-2'-deoxyuridine (BrdU) labelling index (LI) increased from 0.07+/-0.04% before pregnancy to 1.13+/-0.20% at day 12 and decreased thereafter to reach again basal levels at day 21. In PM females, beta-cell proliferation rate was decreased at day 12 (0.74+/-0.15%, P<0.05) but similar to controls at all other stages studied. Separate analysis of the head and tail parts of the pancreas in control animals revealed that the beta-cell fraction during pregnancy increased more in the head than in the tail; similarly, BrdU LI increased 20-fold in the head and 10-fold in the tail, compared with non-pregnant values. In PM females, no adaptation of beta-cell fraction could be observed in the head, where BrdU LI was decreased by half at day 12 of pregnancy. In PM females the lactogenic activity was twice that of controls at day 12 whereas all beta-cells expressed the prolactin receptor. In conclusion, perinatal malnutrition impairs subsequent adaptation to pregnancy by decreasing beta-cell proliferation in the head of the pancreas at a critical time during pregnancy.
