Influence of medroxyprogesterone acetate (Provera) on plasma growth hormone levels and on carbohydrate metabolism

1981 ◽  
Vol 98 (4) ◽  
pp. 603-608 ◽  
Author(s):  
J. E. Eigenmann ◽  
R. Y Eigenmann
Keyword(s):  
Insulin Resistance ◽  
Growth Hormone ◽  
Carbohydrate Metabolism ◽  
Medroxyprogesterone Acetate ◽  
Insulin Response ◽  
The Other ◽  
Combined Effects ◽  
Glucose Load ◽  
Plasma Growth Hormone ◽  
Glucose Assimilation

Abstract. The combined effects of oestradiol and medroxyprogesterone acetate on growth hormone (GH) levels and carbohydrate metabolism were studied in 6 ovariohysterectomized dogs, which previously had shown moderate increments in GH after medroxyprogesterone acetate (MPA) administration. Oestradiol (Oe2) implants were administered 5 months after the last MPA injection, when MPA and GH levels tended to decrease. Following Oe2 administration GH levels rose significantly. Single MPA injections (100 mg) given 20 days after Oe2-priming were followed by still further increased GH levels. These GH levels were several-fold higher than GH levels achieved by previous MPA administration alone. GH levels decreased in 3 dogs after 35 days and remained elevated in the other 3 dogs as long as 70 days after MPA administration with Oe2 priming. Glucose assimilation became impaired and insulin response to a glucose load increased in relation to elevated GH levels. Oe2-primed control dogs, which received no MPA, failed to develop elevated GH levels. These findings indicate (1) that Oe2 and MPA induce overproduction in ovariohysterectomized dogs synergistically (2) that GH levels of the magnitude evoked are associated with glucose intolerance and insulin resistance.

scholarly journals The Interactive Effect of High Doses of Chromium(III) and Different Iron(III) Levels on the Carbohydrate Status, Lipid Profile, and Selected Biochemical Parameters in Female Wistar Rats

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3070
Author(s):  
Halina Zofia Staniek ◽  
Ewelina Król ◽  
Rafał Wojciech Wójciak
Keyword(s):  
Insulin Resistance ◽  
Lipid Profile ◽  
Carbohydrate Metabolism ◽  
Biochemical Parameters ◽  
Wistar Rats ◽  
Interactive Effect ◽  
The Other ◽  
Iron Deficient ◽  
Female Wistar Rats ◽  
High Doses

The aim of the study was to evaluate the main and interactive effects of chromium(III) propionate complex (Cr3) supplementation and different iron supply on the carbohydrate metabolism, lipid profile and other selected biochemical parameters of rats. The experiment was carried out in a two-factor design, in which rats were fed a diet with different proportions of Fe(III) and Cr(III) for six weeks. Fifty-four healthy female Wistar rats were divided into nine experimental groups with different Fe(III) levels, i.e. adequate—control group (45 mg/kg)—100% recommended daily dietary dose of Fe for rodents, deficient (5 mg/kg) and oversupply (180 mg/kg—400%). At the same time they were supplemented with Cr(III) of doses 1 (adequate), 50 and 500 mg/kg of diet. The activity and concentrations of most biochemical parameters were measured with standard enzymatic, kinetic, and colorimetric methods. HOMA-IR and QUICKI indexes were calculated according to appropriate formulas. It was found that there was an interactive effect of high Cr(III) doses and different Fe(III) levels in the diet on the carbohydrate metabolism and insulin resistance indexes. The presented results suggested that iron deficient diet fed animals led to insulin resistance; however, an effect is attenuated by Cr(III) supplementation at high doses. There were no significant changes in the rats’ lipid profile (except for the high density lipoprotein cholesterol (HDL-C) level) and most of the other biochemical parameters, such as the leptin, aspartate aminotransferase (AST), alanine transaminase (ALT), total protein (TP), creatinine (Crea) and the urea (BUN) concentrations. The study proved that the Cr(III) supplementation, independently and in combination with diversified Fe(III) content in the diet, affected the carbohydrate metabolism and insulin resistance indexes but did not affect lipid profile and most of the other biochemical parameters in healthy rats. The findings proved the role of Fe and Cr(III) and their interactions on disturbances carbohydrates metabolism.

Growth hormone-induced insulin resistance: role of the insulin receptor, IRS-1, GLUT-1, and GLUT-4

1997 ◽  
Vol 272 (6) ◽  
pp. E1071-E1079 ◽  
Author(s):  
T. R. Smith ◽  
J. S. Elmendorf ◽  
T. S. David ◽  
J. Turinsky
Keyword(s):  
Insulin Resistance ◽  
Growth Hormone ◽  
Plasma Membrane ◽  
Insulin Receptor ◽  
Insulin Response ◽  
Low Density ◽  
Glut 1 ◽  
Glut 4 ◽  
Fasting Plasma ◽  
Receptor Beta

Treatment of rats with growth hormone (GH; 1 mg/kg sc) twice daily over 2.5 days did not alter fasting plasma glucose or glucose tolerance but increased fasting plasma insulin levels 65% and peak insulin response to a glucose load 35% over controls, indicating the development of insulin resistance. Studies on partially purified insulin receptors from soleus muscles showed that GH increased the abundance of insulin receptor beta-subunits by 48% as measured by immunoblotting. Despite this increase, GH abolished the increase in autophosphorylation of the insulin receptor beta-subunit in response to physiological hyperinsulinemia and diminished by 28% the response to supraphysiological hyperinsulinemia. Similarly, insulin-stimulated phosphorylation of insulin receptor substrate-1 (IRS-1) was decreased 25% by GH, but the abundance of IRS-1 was not affected. Studies on rats pretreated with streptozotocin suggested that the effects of GH are direct and not secondary to GH-induced hyperinsulinemia. GH decreased basal GLUT-1 abundance in the low-density microsome and plasma membrane fractions of epididymal adipocytes by 50 and 42%, respectively, but decreased basal GLUT-4 abundance only in the low-density microsome fraction by 24%. Despite these alterations, the abundance of both transporters in the plasma membrane fraction of adipocytes incubated with 0.1 U insulin/ml was not diminished by GH.

PARTIAL SOMATOTROPHIN INSUFFICIENCY IN CUSHING'S SYNDROME

1969 ◽  
Vol 60 (1) ◽  
pp. 121-129 ◽  
Author(s):  
G. Strauch ◽  
E. Modigliani ◽  
P. Luton ◽  
H. Bricaire
Keyword(s):  
Growth Hormone ◽  
Cushing’S Syndrome ◽  
Selective Inhibition ◽  
Cushing's Syndrome ◽  
Glucose Load ◽  
Plasma Growth Hormone ◽  
Arginine Infusion ◽  
Hormone Levels

ABSTRACT Plasma growth hormone levels were studied in 15 patients with Cushing's syndrome using several stimuli. All tests except one, were performed before treatment. No change occurred in 6 patients during acute hypoglycaemia and in 11 out of 13 after a glucose load. Arginine given intravenously to 11 subjects elicited a rise in 7 out of 8 females and 1 out of 3 males. From patients who responded to arginine infusion, 6 were insensitive to one or two of the above mentioned stimuli. A selective inhibition of the releasing mechanisms might account for the partial somatotrophin insufficiency found in Cushing's syndrome.

scholarly journals Top Single Nucleotide Polymorphisms Affecting Carbohydrate Metabolism in Metabolic Syndrome: From the LIPGENE Study

2014 ◽  
Vol 99 (2) ◽  
pp. E384-E389 ◽  
Author(s):  
Javier Delgado-Lista ◽  
Pablo Perez-Martinez ◽  
Juan Solivera ◽  
Antonio Garcia-Rios ◽  
A. I. Perez-Caballero ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Single Nucleotide Polymorphisms ◽  
Carbohydrate Metabolism ◽  
Insulin Response ◽  
Intravenous Glucose Tolerance Test ◽  
Sensitivity Index ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Intravenous Glucose

Rationale: Metabolic syndrome (MetS) is a high-prevalence condition characterized by altered energy metabolism, insulin resistance, and elevated cardiovascular risk. Objectives: Although many individual single nucleotide polymorphisms (SNPs) have been linked to certain MetS features, there are few studies analyzing the influence of SNPs on carbohydrate metabolism in MetS. Methods: A total of 904 SNPs (tag SNPs and functional SNPs) were tested for influence on 8 fasting and dynamic markers of carbohydrate metabolism, by performance of an intravenous glucose tolerance test in 450 participants in the LIPGENE study. Findings: From 382 initial gene-phenotype associations between SNPs and any phenotypic variables, 61 (16% of the preselected variables) remained significant after bootstrapping. Top SNPs affecting glucose metabolism variables were as follows: fasting glucose, rs26125 (PPARGC1B); fasting insulin, rs4759277 (LRP1); C-peptide, rs4759277 (LRP1); homeostasis assessment of insulin resistance, rs4759277 (LRP1); quantitative insulin sensitivity check index, rs184003 (AGER); sensitivity index, rs7301876 (ABCC9), acute insulin response to glucose, rs290481 (TCF7L2); and disposition index, rs12691 (CEBPA). Conclusions: We describe here the top SNPs linked to phenotypic features in carbohydrate metabolism among approximately 1000 candidate gene variations in fasting and postprandial samples of 450 patients with MetS from the LIPGENE study.

CARBOHYDRATE METABOLISM IN KLINEFELTER'S SYNDROME

1966 ◽  
Vol 35 (2) ◽  
pp. 169-172 ◽  
Author(s):  
I. M. D. JACKSON ◽  
K. D. BUCHANAN ◽  
M. T. McKIDDIE ◽  
C. R. M. PRENTICE
Keyword(s):  
Carbohydrate Metabolism ◽  
Insulin Response ◽  
Oral Glucose ◽  
Klinefelter’S Syndrome ◽  
Oral Glucose Tolerance ◽  
Glucose Load ◽  
Klinefelter's Syndrome ◽  
Glucose Tolerance Curve ◽  
Plasma Insulin Levels ◽  
Tolerance Curve

SUMMARY Carbohydrate metabolism has been investigated in eight patients with Klinefelter's syndrome. Seven of the eight had a normal oral glucose tolerance curve; one patient had slightly impaired tolerance. Plasma insulin levels were measured in response to the glucose load and were normal in six and slightly abnormal in two patients; one of the latter had an early increased and the other a delayed insulin response. No definite conclusions are reached regarding the possibility of a significant association between Klinefelter's syndrome and diabetes mellitus.

PLASMA GROWTH HORMONE IN CHILDREN AT NIGHT AND FOLLOWING A GLUCOSE LOAD

1965 ◽  
Vol 49 (3_Suppl) ◽  
pp. S121 ◽  
Author(s):  
W. M. Hunter ◽  
W. M. Rigal
Keyword(s):  
Growth Hormone ◽  
Glucose Load ◽  
Plasma Growth Hormone

Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity

1996 ◽  
Vol 135 (2) ◽  
pp. 205-210 ◽  
Author(s):  
Mauro Maccario ◽  
Silvia Grottoli ◽  
Paola Razzore ◽  
Massimo Procopio ◽  
Salvatore Endrio Oleandri ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Growth Hormone ◽  
Insulin Secretion ◽  
Body Mass ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Insulin Response ◽  
Glucose Load ◽  
Gh Secretion ◽  
Glucose Levels

Maccario M, Grottoli S, Razzore P, Procopio M, Oleandri SE, Ciccarelli E, Camanni F, Ghigo E. Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity. Eur J Endocrinol 1996;135:205–10. ISSN 0804–4643 In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition. In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18–46 years, body mass index = 21.8 ± 0.6 kg/m2, basal prolactin = 91.7 ± 16.5 μg/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23–48 years, body mass index = 38.3 ± 2.6 kg/m2) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26–32 years, body mass index = 20.6 ± 1.9 kg/m2) were studied as controls. The insulin response to glucose in HP (area under curve = 11460.8 ± 1407.5 mU·min·1−1) was not significantly different from NS (7743.7 ±882.9 mU·min·1−1) and OB (14 504.8 ± 1659.9 mU·min·1−1). The arginine-induced insulin release in HP and OB was similar (4219.4 ± 631.7 and 4107.3 ± 643.2 mU·min·1−1. respectively), both being higher (p < 0.02) than in NS (2178.1 ± 290.9 mU·min·1−1). Glucose and arginine had an additive effect on insulin release in HP and NS (19 769.1 ± 3249.6 and 10996.6 ± 1201.0 mU·min·1−1, respectively) and a synergistic effect in OB (28117.3± 5224.7 mU·min·1−1). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in HP and NS. Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in HP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion. The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely. Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy

Plasma growth hormone and insulin response to levodopa and amantadine

1973 ◽  
Vol 34 (2) ◽  
pp. 145-151 ◽  
Author(s):  
O. Kyt�m�ki ◽  
R. Nousiainen ◽  
A. Pekkarinen ◽  
U. K. Rinne ◽  
M. Viljanen
Keyword(s):  
Growth Hormone ◽  
Insulin Response ◽  
Plasma Growth Hormone
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