Introduction It has been well established that abnormal elevation in circulating glucagon leads to an increase in hepatic glucose production and glycogen metabolism that contribute to hyperglycaemia in diabetes ( Unger 1978 ). For this reason
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Ryan A Lafferty, Laura M McShane, Zara J Franklin, Peter R Flatt, Finbarr P M O’Harte, and Nigel Irwin
Tusty-Jiuan Hsieh, Pierre Fustier, Chih-Chang Wei, Shao-Ling Zhang, Janos G Filep, Shiow-Shiu Tang, Julie R Ingelfinger, I George Fantus, Pavel Hamet, and John S D Chan
, however, that hyperglycaemia and RAS activation are major determinants of diabetic nephropathy. Angiotensinogen is the sole substrate of the RAS. It is now well accepted that there is a local intrarenal RAS ( Dzau & Ingelfinger 1989 , Johnston et
Antonia Giacco, Teresa Peluso, Federica Cioffi, Stefania Iervolino, Giovanna Mercurio, Luca Roberto, Carla Reale, Marco Colella, Mario De Felice, Maria Moreno, Concetta Ambrosino, and Elena Silvestri
, exhibit net fasting hyperglycaemia (+33% vs Wt) ( Fig. 3A ) and hyperinsulinemia (+80% vs Wt) ( Fig. 3B ) as well as increased HOMA-IR index ( Fig. 3C ). DHTP mice show a slight but not significant increase in fasting glycaemia (+29% vs wild type
ANITA PAKRASHI and SAMIR K. MUKHERJEE
SUMMARY
Oral administration of 250 mg hydrochlorothiazide/kg, with previous i.v. injection of 4 i.u. soluble insulin or s.c. injection of protamine-zinc insulin, has been found to produce stable hyperglycaemia in rabbits irrespective of sex. It is thought that insulin helps the selective action of hydrochlorothiazide on the β cells by removing the protective glucose barrier. Although stimulation of glucagon or some extra-pancreatic mechanism at the initial stage could not be altogether ruled out, the central action of the drug is supported by the finding that the hydrochlorothiazide-induced hyperglycaemia was lowered by the sulphonylurea derivative, chlorpropamide.
Bernadette M Trojanowski, Heba H Salem, Heike Neubauer, Eric Simon, Martin Wagner, Rajkumar Dorajoo, Bernhard O Boehm, Leticia Labriola, Thomas Wirth, and Bernd Baumann
hyperglycaemia or glucose intolerance. Furthermore, differences concerning disease severity and therapy response can be observed ( Fajans & Bell 2011 , Bansal et al. 2017 , Hattersley & Patel 2017 , Owen 2018 ). Interestingly, phenotypic heterogeneity is
Meng Guo, Yuna Li, Yan Wang, Zhenkun Li, Xiaohong Li, Peikun Zhao, Changlong Li, Jianyi Lv, Xin Liu, Xiaoyan Du, and Zhenwen Chen
hyperglycaemia, impaired glucose tolerance and diabetic pathophysiological lesions ( Li et al. 2016 ). Using suppression subtractive hybridisation (SSH), eukaryotic translation elongation factor 1 alpha ( Eef1a2 ) was selected as one of the DE genes in the
K S Wilson, C S Tucker, E A S Al-Dujaili, M C Holmes, P W F Hadoke, C J Kenyon, and M A Denvir
adults with tissue-specific alterations to Gr mRNA expression, including t is associated in adults with tissue-specific alterations he liver, leading to hepatic expression of the gluconeogenic enzyme pepck and hyperglycaemia. Although blood glucose
S. HARVEY, C. G. SCANES, A. CHADWICK, and N. J. BOLTON
The concentrations of both GH and prolactin in the circulation of the domestic fowl have been determined after various treatments known to affect carbohydrate metabolism. Fasting decreased the level of glucose, stimulated the secretion of GH and inhibited the secretion of prolactin. Administration of insulin significantly depressed the level of GH in the plasma of normal or fasted birds and also in chickens which had received simultaneous injections of glucose or 2-deoxy-d-glucose. No consistent effect of insulin on the secretion of prolactin was observed. Hyperglycaemia subsequent to administration of glucose had no effect on the levels of either GH or prolactin. Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin.
F. MASSARA and E. STRUMIA
SUMMARY
Plasma human growth hormone (HGH) concentrations were compared during four tests in which 0·9% NaCl solution only, propranolol, adrenaline or propranolol plus adrenaline were infused into six healthy volunteers. In five subjects, HGH levels during the infusion of saline, propranolol or adrenaline showed no significant increase and were virtually identical. During the test with propranolol plus adrenaline, however, there was an increase after adrenaline in spite of concomitant hyperglycaemia. The sixth volunteer showed a wide range of apparently spontaneous and irregular variations in HGH values throughout each of the four tests.
These findings support the view that α-receptors stimulate and β-receptors depress HGH secretion, and show that adrenergically stimulated HGH secretion in man is not inhibited by hyperglycaemia.
I. K. Martin and I. R. McDonald
ABSTRACT
In a study of adrenocortical functions in macropodid marsupials, measurements were made of the effects of ACTH infusion, ether stress and adrenaline infusion on plasma corticosteroid and glucose concentrations in wallabies (Thylogale billardierii) provided with indwelling venous catheters.
The mean plasma total glucocorticoid concentration in undisturbed males and females was 80 ± 5 (s.e.m.) μg/l, of which more than 90% was cortisol. This fraction declined to 68% of the total at the highest ACTH-stimulated concentration of 225 μg/l, due to an increase in the contribution by 11-deoxycortisol.
Although maximal ACTH stimulation (4·5 i.u./kg per h) caused a five- to sixfold increase in cortisol secretion rate, as measured by isotope dilution during constant-rate tracer infusion, plasma cortisol concentration rose only two- to threefold, due to a marked increase in metabolic clearance.
Plasma glucose concentration did not change significantly during either short-term (1 h) i.v. infusion or long-term (8 days) i.m. injection of ACTH, even though plasma cortisol concentration was significantly increased.
Ether anaesthesia caused a marked hyperglycaemia that preceded an increase in plasma cortisol concentration and was not sustained while plasma cortisol concentration continued to increase.
Infusion of adrenaline i.v. at rates sufficient to cause a similar hyperglycaemia had no significant effect on plasma cortisol concentration. A marked hyperglycaemia during xylazine anaesthesia was not associated with an increase in plasma cortisol concentration and was attributable to suppression of insulin secretion.
It is concluded that, as in the red kangaroo (Macropus rufus) and the quokka (Setonix brachyurus) and in contrast to the reported effects in the tammar wallaby (Macropus eugenii), neither ACTH, nor the increase in plasma glucocorticoid concentration caused by ACTH administration, influence plasma glucose concentration in Thylogale billardierii.
J. Endocr. (1986) 110, 471–480
