diabetestalk.net

Growth Hormone Deficiency Insulin Resistance

Effects Of Growth Hormone On Diurnal Insulin Sensitivity In Normal And Type 2 Diabetic Patients And Animal Models

Effects Of Growth Hormone On Diurnal Insulin Sensitivity In Normal And Type 2 Diabetic Patients And Animal Models

1Division of Endocrinology and Metabolism, Department of Medicine, Cheng Hsin General Hospital, Taipei 112, Taiwan 2Division of Endocrinology and Metabolism, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan 3School of Medicine, National Yang-Ming University, Taipei 112, Taiwan 4Department of Medical Research, Taipei-Veterans General Hospital, Taipei 112, Taiwan *Corresponding Author: Kuang-Chung Shih Division of Endocrinology and Metabolism Department of Medicine Cheng Hsin General Hospital Taipei 112, Taiwan Tel: +886-2-28264400 Fax: +886-2-27356005 E-mail: [email protected] Citation: Shih KC, Ho LT (2016) Effects of Growth Hormone on Diurnal Insulin Sensitivity in Normal and Type 2 Diabetic Patients and Animal Models. J Diabetes Metab 7:709. doi:10.4172/2155-6156.1000709 Copyright: © 2016 Shih KC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract This review addresses the effects of growth hormone on diurnal insulin sensitivity in normal, patients with type 2 diabetes mellitus (T2DM) and animal models described in our previous studies. Results confirmed the presence of diurnal insulin sensitivity, or greater insulin sensitivity in the morning, in normal subjects. The exact cause of this circadian rhythm in plasma glucose levels in healthy subjects has not been established, and nocturnal surges in growth hormone secretion remain a possible explanation. Results showed that growth hormone is an important factor controlling the diurnal variation of glucose tolerance and Continue reading >>

Insulin Inhibits Growth Hormone Signaling Via The Growth Hormone Receptor/jak2/stat5b Pathway*

Insulin Inhibits Growth Hormone Signaling Via The Growth Hormone Receptor/jak2/stat5b Pathway*

Bovine GH (bGH; lot number APF11182B) and ovine prolactin (oPRL, NIDDK-oPRL-21; lot number AFP-10692C) were kindly provided by Dr. A. F. Parlow, Pituitary Hormones and Antisera Center, Harbor-UCLA Medical Center (Torrance, CA) and the NIDDK, National Institutes of Health National Hormone & Pituitary Program. The125I-human GH (125I-hGH) was purchased from NENTM Life Science Products. Porcine sodium-insulin was a gift from Dr. Ron Chance (Eli Lilly, Co., Indianapolis, IN) and unlabeled hGH was also kindly provided by Eli Lilly, Co. Fetal bovine serum, calf serum, and horse serum were purchased from Life Technologies, Inc. (Grand Island, NY). Protein G-Sepharose was obtained from Pharmacia Biotech Inc. (Uppsala, Sweden) and ECL detection reagents were obtained from Amersham Corp. Other materials were purchased from Sigma and Fisher (Pittsburgh, PA) unless otherwise noted. Anti-STAT5 monoclonal antibody (raised against amino acid 451649 of sheep STAT5A) was purchased from Transduction Laboratories (Lexington, KY). Mouse anti-STAT5A (raised against the unique C terminus of murine STAT5A) and mouse anti-STAT5B (raised against the unique C terminus of murine STAT5B) monoclonal antibodies and rabbit anti-phosphotyrosine-STAT5 polyclonal antibodies (raised against the phospho-peptide around C-terminal Y694 of murine STAT5A that is conserved in both STAT5A and STAT5B of human, sheep, and rat) were obtained from Zymed Laboratories Inc. (San Francisco, CA). Rabbit anti-JAK2 peptide antiserum, directed at residues 758776 of murine JAK2 (called anti-JAK2UBI), and 4G10 mouse monoclonal anti-phosphotyrosine antibody were purchased from Upstate Biotechnology, Inc. (Lake Placid, NY). A second anti-JAK2 serum (anti-JAK2AL33) was raised in rabbits against a glutathioneS-transferase fusion Continue reading >>

Growth Hormone (gh)-induced Insulin Resistance Is Rapidly Reversible: An Experimental Study In Gh-deficient Adults

Growth Hormone (gh)-induced Insulin Resistance Is Rapidly Reversible: An Experimental Study In Gh-deficient Adults

The Journal of Clinical Endocrinology & Metabolism Growth Hormone (GH)-Induced Insulin Resistance Is Rapidly Reversible: An Experimental Study in GH-Deficient Adults Department of Internal Medicine and Endocrinology and Medical Research Laboratories (T.K.-H., N.M., S.B.P., J.S.C., J.O.L.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Address all correspondence and requests for reprints to: Thomas Krusenstjerna-Hafstrm, M.D., Department of Internal Medicine and Endocrinology and Medical Research Laboratories, Aarhus University Hospital, Nrrebrogade 44, 8000 Aarhus C, Denmark. Search for other works by this author on: Department of Clinical Pharmacology (B.F.C., N.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Search for other works by this author on: Department of Internal Medicine and Endocrinology and Medical Research Laboratories (T.K.-H., N.M., S.B.P., J.S.C., J.O.L.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Search for other works by this author on: Department of Clinical Pharmacology (B.F.C., N.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Search for other works by this author on: Department of Internal Medicine and Endocrinology and Medical Research Laboratories (T.K.-H., N.M., S.B.P., J.S.C., J.O.L.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Search for other works by this author on: Department of Internal Medicine and Endocrinology and Medical Research Laboratories (T.K.-H., N.M., S.B.P., J.S.C., J.O.L.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Search for other works by this author on: Department of Internal Medicine and Endocrinology and Medical Research Laboratories (T.K.-H., N.M., S.B.P., J.S.C., J.O.L.J.), Aarhus University Hospital, 8000 Aarhus C, Denmark Search for other works by this author o Continue reading >>

Effects Of Growth Hormone On Glucose Metabolism And Insulin Resistance In Human

Effects Of Growth Hormone On Glucose Metabolism And Insulin Resistance In Human

Effects of growth hormone on glucose metabolism and insulin resistance in human Kim and Park: Effects of growth hormone on glucose metabolism and insulin resistance in human Annals of Pediatric Endocrinology & Metabolism 2017;22(3): 145-152. Department of Pediatrics, Inje University Sanggye Paik Hospital, Seoul, Korea Address for correspondence: Mi-Jung Park, MD, PhD Department of Pediatrics, Inje University Sanggye Paik Hospital, 1342 Dongilro, Nowon-gu, Seoul 01767, Korea Tel: +82-2-950-8826 Fax: +82-2-950-1246 E-mail: [email protected] Received August 31, 2017 Accepted September 11, 2017 2017 Annals of Pediatric Endocrinology & Metabolism This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Growth hormone (GH) is important for promotion of somatic growth and the regulation of substrate metabolism. Metabolic action of GH occurs in multiple tissues including the liver, muscle, fat and pancreas either directly or indirectly through insulin-like growth factor 1. The diabetogenic action of GH has been well-described in previous in vivo studies. In this paper, we review the metabolic effects of GH on peripheral tissues focusing on glucose metabolism and insulin resistance, and discuss results from human studies on the long-term effects of GH administration on insulin resistance and hyperglycemia. Keywords: Growth hormone , Glucose , Metabolism , Insulin resistance Glucose balance in circulation is tightly maintained within normal range by dynamic regulation of both glucose production (from liver and kidney) and glucose usage by peripheral tissues including the liver, mus Continue reading >>

Insulin Resistance In Growth Hormone-deficient Adults: Defects In Glucose Utilization And Glycogen Synthase Activity.

Insulin Resistance In Growth Hormone-deficient Adults: Defects In Glucose Utilization And Glycogen Synthase Activity.

Insulin resistance in growth hormone-deficient adults: defects in glucose utilization and glycogen synthase activity. Hew FL, et al. J Clin Endocrinol Metab. 1996. Department of Endocrinology and Diabetes, St. Vincent's Hospital, Fitzroy, Melbourne, Victoria, Australia. J Clin Endocrinol Metab. 1996 Feb;81(2):555-64. Fourteen GH-deficient (GHD) adults were compared with 12 age-, sex-, and body mass index-matched control subjects using a baseline tritiated glucose equilibration period and euglycemic-hyperinsulinemic (approximately 55 mU/L) clamp in conjunction with paired muscle biopsies for measurement of glycogen synthase fractional velocity (FV0.1). Despite similar basal rates of total glucose disposal (Rd), there was a 64% reduction in the insulin-stimulated rise (delta) in Rd in the GHD adults compared to that in controls [16.6 +/- 2.8 vs. 44.7 +/- 6.0 mumol/kg fat free mass (FFM)/min; P < 0.001], which was mainly due to a decreased glucose storage (GS) rate (delta GS, 12.6 +/- 2.9 vs. 39.5 +/- 7.5 mumol/kg FFM/min; P < 0.01). Furthermore, the insulin sensitivity indexes of Rd (0.39 +/- 0.07 vs. 0.85 +/- 0.11; P < 0.05) and GS (0.25 +/- 0.07 vs. 0.72 +/- 0.13 mumol/kg FFM/min per mU/L; P < 0.02) were reduced in GHD adults compared to the control values. The insulin sensitivity of the glycolytic pathway was also reduced by approximately 50% in GHD adults (P = 0.07 vs. controls). Insulin-stimulated FV0.1 was decreased in GHD adults (0.31 +/- 0.02 vs. 0.47 +/- 0.03; P < 0.005) despite similar basal FV0.1. Using multiple and stepwise regression analysis, duration of GH deficiency, fasting triglycerides and fasting insulin accounted for 67% of the variance in the insulin sensitivity index of Rd. In conclusion, the severe insulin resistance in GHD adults is mainly due to Continue reading >>

Frontiers | Growth Hormone, Insulin-like Growth Factor-1, Insulin Resistance, And Leukocyte Telomere Length As Determinants Of Arterial Aging In Subjects Free Of Cardiovascular Diseases | Genetics

Frontiers | Growth Hormone, Insulin-like Growth Factor-1, Insulin Resistance, And Leukocyte Telomere Length As Determinants Of Arterial Aging In Subjects Free Of Cardiovascular Diseases | Genetics

Front. Genet., 15 December 2017 | Growth Hormone, Insulin-Like Growth Factor-1, Insulin Resistance, and Leukocyte Telomere Length as Determinants of Arterial Aging in Subjects Free of Cardiovascular Diseases 1Department of Clinical Cardiology and Molecular Genetics, Federal State Institution National Medical Research Center for Preventive Medicine of the Ministry of Healthcare of the Russian Federation, Moscow, Russia 2Department of Age-associated Diseases, Medical Scientific and Educational Center, Lomonosov Moscow State University, Moscow, Russia 3Russian Clinical Research Center for Gerontology, Pirogov Russian National Research Medical University, Moscow, Russia 4Department of Fundamental and Applied Aspects of Obesity, Federal State Institution National Medical Research Center for Preventive Medicine of the Ministry of Healthcare of the Russian Federation, Moscow, Russia 5Department of Cardiology, Federal Scientific and Clinical Center of the Federal Medico-Biological Agency, Moscow, Russia 6Department of Aging and Age-associated Diseases Prevention, Federal State Institution National Medical Research Center for Preventive Medicine of the Ministry of Healthcare of the Russian Federation, Moscow, Russia 7Department of Primary Prevention of Chronic Non-Communicable Diseases in the Healthcare System, Federal State Institution National Medical Research Center for Preventive Medicine of the Ministry of Healthcare of the Russian Federation, Moscow, Russia 8Biobank, Federal State Institution National Medical Research Center for Preventive Medicine of the Ministry of Healthcare of the Russian Federation, Moscow, Russia 9Department of Epidemiology of Chronic Non-Communicable Diseases Laboratory of Biostatistics, Federal State Institution National Medical Research Center fo Continue reading >>

Growth Hormone Deficiency And Insulin Sensitivity

Growth Hormone Deficiency And Insulin Sensitivity

Growth Hormone Deficiency and Insulin Sensitivity Growth Hormone Deficiency and Insulin Sensitivity The human body is an extremely complex organism that depends on hormones for much of its functions. Insulin and growth hormone are both important to the bodys metabolism. The hormones in the human body dont exist in isolation; nearly all interact with each other either directly or indirectly. Growth hormone and insulin are two of the hormones that are directly related to each other. In the case of these two important hormones, a deficiency in human growth hormone (HGH) can affect your bodys sensitivity to insulin. This has important implications for those who have growth hormone deficiency and are trying to lose weight, or who have prediabetes and diabetes. As you might guess from the name, HGH is what causes children and adolescents to grow. Produced by the pituitary gland, the level of this hormone fluctuates throughout life. In adults, it is important because it helps regulate body composition, muscle and bone growth. Useful Articles: HGH for Women ; HGH for Men It helps balance body fluids and affects sugar and fat metabolism. It may also affect heart function. When deficient in childhood, lack of HGH can lead to growth failure and dwarfism. Growth hormone levels are naturally highest during the growth spurt of puberty and gradually decrease as people age. However, some people can also become deficient in this important hormone in adulthood. In adults, HGH deficiency is more likely to result in decreased muscle mass, problems with bone density and psychological symptoms such as depression, social withdrawal and difficulty remembering things. When HGH decifiency occurs in adulthood, it is not that the body decreases production so much as that less is released into the Continue reading >>

Growth Hormone-induced Insulin Resistance Is Associated With Increased Intramyocellular Triglyceride Content But Unaltered Vldl-triglyceride Kinetics

Growth Hormone-induced Insulin Resistance Is Associated With Increased Intramyocellular Triglyceride Content But Unaltered Vldl-triglyceride Kinetics

Growth hormone-induced insulin resistance is associated with increased intramyocellular triglyceride content but unaltered VLDL-triglyceride kinetics The ability of growth hormone (GH) to stimulate lipolysis and cause insulin resistance in skeletal muscle may be causally linked, but the mechanisms remain obscure. We investigated the impact of GH on the turnover of FFA and VLDL-TG, intramuscular triglyceride content (IMTG), and insulin sensitivity (euglycemic clamp) in nine healthy men in a randomized double-blind placebo-controlled crossover study after 8 days treatment with (A) Placebo + Placebo, (B) GH (2 mg daily) + Placebo, and (C) GH (2 mg daily) + Acipimox (250 mg 3 daily). In the basal state, GH (B) increased FFA levels (P < 0.05), palmitate turnover (P < 0.05), and lipid oxidation (P = 0.05), but VLDL-TG kinetics were unaffected. Administration of acipimox (C) suppressed basal lipolysis but did not influence VLDL-TG kinetics. In the basal state, IMTG content increased after GH (B; P = 0.03). Insulin resistance was induced by GH irrespective of concomitant acipimox (P < 0.001). The turnover of FFA and VLDL-TG was suppressed by hyperinsulinemia during placebo and GH, whereas coadministration of acipimox induced a rebound increase FFA turnover and VLDL-TG clearance. We conclude that these results show that GH-induced insulin resistance is associated with increased IMTG and unaltered VLDL-TG kinetics; we hypothesize that fat oxidation in muscle tissue is an important primary effect of GH and that circulating FFA rather than VLDL-TG constitute the major source for this process; and the role of IMTG in the development of GH-induced insulin resistance merits future research. a reproducible effect of growth hormone (GH) is mobilization of body fat and stimulation of li Continue reading >>

Growth Hormone Replacement Therapy Induces Insulin Resistance By Activating The Glucose-fatty Acid Cycle

Growth Hormone Replacement Therapy Induces Insulin Resistance By Activating The Glucose-fatty Acid Cycle

Growth Hormone Replacement Therapy Induces Insulin Resistance by Activating the Glucose-Fatty Acid Cycle Department of Endocrinology (M.B., M.S., E.L., P.M., L.G.), University Hospital, S-205 02 Malmo, Sweden; Address all correspondence and requests for reprints to: Margareta Bramnert, Department of Endocrinology, University Hospital MAS, S-205 +2 Malmo, Sweden. Search for other works by this author on: Department of Endocrinology (M.B., M.S., E.L., P.M., L.G.), University Hospital, S-205 02 Malmo, Sweden; Search for other works by this author on: Department of Endocrinology (M.B., M.S., E.L., P.M., L.G.), University Hospital, S-205 02 Malmo, Sweden; Search for other works by this author on: Copenhagen Muscle Research Centre (J.R.D.), Department of Human Physiology, DK-2100 Copenhagen, Denmark Search for other works by this author on: Department of Endocrinology (M.B., M.S., E.L., P.M., L.G.), University Hospital, S-205 02 Malmo, Sweden; Search for other works by this author on: Department of Endocrinology (M.B., M.S., E.L., P.M., L.G.), University Hospital, S-205 02 Malmo, Sweden; Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 4, 1 April 2003, Pages 14551463, Margareta Bramnert, Mikael Segerlantz, Esa Laurila, Jens R. Daugaard, Per Manhem, Leif Groop; Growth Hormone Replacement Therapy Induces Insulin Resistance by Activating the Glucose-Fatty Acid Cycle, The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 4, 1 April 2003, Pages 14551463, The effects of GH replacement therapy on energy metabolism are still uncertain, and long-term benefits of increased muscle mass are thought to outweigh short-term negative metabolic effects. This study was designed to address this issue by examining both Continue reading >>

Evaluation Of Insulin Sensitivity In Growth Hormone (gh) Deficient Children Before And At The End Of Rhgh Therapy

Evaluation Of Insulin Sensitivity In Growth Hormone (gh) Deficient Children Before And At The End Of Rhgh Therapy

Evaluation of insulin sensitivity in growth hormone (GH) deficient children before and at the end of rhGH therapy Silvia Savastio1, Simonetta Bellone1, Jaele Bellone1, Fiorella Zanetta1, Giuseppina Di Dio1, Sara Giacoma1, Antonella Petri1, Flavia Prodam1, Ginevra Corneli1, Gianni Bona1 & Gianluca Aimaretti2 1Division of Pediatrics, University of Piemonte Orientale, Novara, Italy; 2Division of Endocrinology, Department of Clinical and Experimental Medicine, University of Piemonte Orientale, Novara, Italy. Introduction: Therapy with recombinant GH (rhGH) allows GH-deficient children (GHD) to reach an adequate adult stature. Previous studies have reported a significant rise in serum insulin levels during GH therapy. It has been demonstrated that insulin resistance is a risk factor for the development of DMT2, atherosclerosis, dyslipidemia and hypertension. Subjects and methods: Aim of our study was to evaluate changes in insulin sensitivity in a group of GHD children longitudinally followed during rhGH treatment. We measured fasting glucose and insulin levels and after oral glucose tolerance test (OGTT) in 11 GHD children (seven males and four females) at three times: 1) before starting of GH therapy (BT); 2) during the last year of therapy (T1); 3) 6 months (T6) after stopped therapy. At BT children presented age of 9.20.7 years, height SDS 1.90.2, while during T1 age was 15.40.3 years, height SDS 1.20.2. GH treatment was administered subcutaneously at a mean dosage of 0.20.3 mg/kg per week. Results: No children showed impaired glucose tolerance or DMT2 during the therapy. Basal glucose levels were similar among the three times. Glucose levels in response to OGTT were statistically higher at T1 compared to BT and T6 (P<0.007). Fasting and during OGTT insulin levels were Continue reading >>

Growth Hormone-deficient Adults Are Insulin-resistant

Growth Hormone-deficient Adults Are Insulin-resistant

Get rights and content Patients with growth hormone deficiency (GHD) have traditionally been described as having increased insulin sensitivity with a tendency toward fasting hypoglycemia, at least in children. In other studies, impaired glucose tolerance has been found. To evaluate basal insulin sensitivity, a hyperinsulinemic, normoglycemic clamp was performed with an insulin infusion rate of 40 mU/m2/min after an overnight fast. Fifteen patients (four women and 11 men aged 20 to 62 years) with GHD for at least 1 year were compared with 15 healthy controls matched for sex, age, and body mass index (BMI). Thirteen patients had complete pituitary deficiency and were being treated with conventional hormone replacement therapy. Two men had isolated GHD since childhood. Four men were being treated with bromocriptin. There were no significant differences between fasting blood glucose (4.4 0.1 v 4.7 0.2 [mean SEM] mmol/L) or fasting plasma insulin (9.5 1.4 v 8.8 1.1 mU/L) in patients and controls, respectively. Fasting free fatty acid (FFA) levels were lower in patients (444 35 v 796 94 mol/L, P < .01). Blood glucose levels during the clamp were similar (4.6 0.1 v 4.9 0.1 mmol/L), as were insulin levels (81 4 v 93 4 mU/L). A decrease in glucose infusion rate (GIR) was seen during the clamp in GHD subjects (3.9 0.5 v 9.9 0.7 mg/kg body weight/min) as compared with controls (P = .001). Even if corrections were made for body fat, there was a significant difference (GIR corrected per lean body mass, 5.8 0.8 v 13.9 0.9 mg/kg lean body mass/min, P < .001). The results suggest that adults with GHD are insulin-resistant. Despite this finding, normal fasting plasma insulin levels were seen. Continue reading >>

Growth Hormone Deficiency

Growth Hormone Deficiency

Growth hormone deficiency (GHD) is a medical condition due to not enough growth hormone (GH). [3] Generally the most noticeable symptom is a short height . [1] In newborns there may be low blood sugar or a small penis . [2] In adults there may be decreased muscle mass, high cholesterol levels , or poor bone density . [1] GHD can be present at birth or develop later in life. [1] Causes may include genetics , trauma, infections, tumors , or radiation therapy . [2] Genes that may be involved include GH1 , GHRHR , or BTK . [3] In a third of cases no cause is apparent. [2] The underlying mechanism generally involves problems with the pituitary gland . [2] Some cases are associated with a lack of other pituitary hormones , in which case it is known as combined pituitary hormone deficiency . [4] Diagnosis involves blood tests to measure growth hormone levels. [2] Treatment is by growth hormone replacement . [1] The frequency of the condition is unclear. [2] Most cases are initially noticed in children. [1] The genetic forms are estimates to affect about 1 in 7,000 people. [3] Most types occur equally in males and females though males are more often diagnosed. [2] Growth hormone deficiency can be congenital or acquired in childhood or adult life. It can be partial or complete. It is usually permanent, but sometimes transient. It may be an isolated deficiency or occur in association with deficiencies of other pituitary hormones. The term hypopituitarism is often used interchangeably with GH deficiency but more often denotes GH deficiency plus deficiency of at least one other anterior pituitary hormone. When GH deficiency (usually with other anterior pituitary deficiencies) is associated with posterior pituitary hormone deficiency (usually diabetes insipidus ), the condition is Continue reading >>

Insulin Resistance In Growth Hormone-deficient Adults: Defects In Glucose Utilization And Glycogen Synthase Activity

Insulin Resistance In Growth Hormone-deficient Adults: Defects In Glucose Utilization And Glycogen Synthase Activity

Fourteen GH-deficient (GHD) adults were compared with 12 age-, sex-, and body mass index-matched control subjects using a baseline tritiated glucose equilibration period and euglycemic-hyperinsulinemic (approximately 55 mU/L) clamp in conjunction with paired muscle biopsies for measurement of glycogen synthase fractional velocity (FV0.1). Despite similar basal rates of total glucose disposal (Rd), there was a 64% reduction in the insulin-stimulated rise (delta) in Rd in the GHD adults compared to that in controls [16.6 +/- 2.8 vs. 44.7 +/- 6.0 mumol/kg fat free mass (FFM)/min; P < 0.001], which was mainly due to a decreased glucose storage (GS) rate (delta GS, 12.6 +/- 2.9 vs. 39.5 +/- 7.5 mumol/kg FFM/min; P < 0.01). Furthermore, the insulin sensitivity indexes of Rd (0.39 +/- 0.07 vs. 0.85 +/- 0.11; P < 0.05) and GS (0.25 +/- 0.07 vs. 0.72 +/- 0.13 mumol/kg FFM/min per mU/L; P < 0.02) were reduced in GHD adults compared to the control values. The insulin sensitivity of the glycolytic pathway was also reduced by approximately 50% in GHD adults (P = 0.07 vs. controls). Insulin-stimulated FV0.1 was decreased in GHD adults (0.31 +/- 0.02 vs. 0.47 +/- 0.03; P < 0.005) despite similar basal FV0.1. Using multiple and stepwise regression analysis, duration of GH deficiency, fasting triglycerides and fasting insulin accounted for 67% of the variance in the insulin sensitivity index of Rd. In conclusion, the severe insulin resistance in GHD adults is mainly due to the inhibition of the GS pathway and glycogen synthase activity in peripheral tissues, which is related to the duration of GH deficiency, fasting triglycerides, and fasting insulin. Do you want to read the rest of this article? ... 9,10,[14][15][16] In cases of GH deficiency, there will be increased insulin sensitivi Continue reading >>

Growth Hormone-deficient Adults Are Insulin-resistant.

Growth Hormone-deficient Adults Are Insulin-resistant.

Growth hormone-deficient adults are insulin-resistant. Johansson JO(1), Fowelin J, Landin K, Lager I, Bengtsson BA. (1)Department of Medicine, Sahlgrenska University Hospital, Gteborg University, Sweden. Patients with growth hormone deficiency (GHD) have traditionally been describedas having increased insulin sensitivity with a tendency toward fastinghypoglycemia, at least in children. In other studies, impaired glucose tolerance has been found. To evaluate basal insulin sensitivity, a hyperinsulinemic,normoglycemic clamp was performed with an insulin rate of 40 mU/m2/min after anovernight fast. Fifteen patients (four women and 11 men aged 20 to 62 years) withGHD for at least 1 year were compared with 15 healthy controls matched for sex,age, and body mass index (BMI). Thirteen patients had complete pituitarydeficiency and were being treated with conventional hormone replacement therapy. Two men had isolated GHD since childhood. Four men were being treated withbromocriptin. There were no significant differences between fasting blood glucose(4.4 +/- 0.1 v 4.7 +/- 0.2 [mean +/- SEM] mmol/L) or fasting plasma insulin (9.5 +/- 1.4 v 8.8 +/- 1.1 mU/L) in patients and controls, respectively. Fasting free fatty acid (FFA) levels were lower in patients (444 +/- 35 v 796 +/- 94 mumol/L, P < .01). Blood glucose levels during the clamp were similar (4.6 +/- 0.1 v 4.9+/- 0.1 mmol/L), as were insulin levels (81 +/- 4 v 93 +/- 4 mU/L). A decrease inglucose infusion rate (GIR) was seen during the clamp in GHD subjects (3.9 +/-0.5 v 9.9 +/- 0.7 mg/kg body weight/min) as compared with controls (P = .001).Even if corrections were made for body fat, there was a significant difference(GIR corrected per lean body mass, 5.8 +/- 0.8 v 13.9 +/- 0.9 mg/kg lean bodymass/min, P < .001). The resul Continue reading >>

Increased Insulin Sensitivity In Young, Growth Hormone Deficient Children.

Increased Insulin Sensitivity In Young, Growth Hormone Deficient Children.

Increased insulin sensitivity in young, growth hormone deficient children. Husbands S, et al. Clin Endocrinol (Oxf). 2001. Department of Endocrinology, Radcliffe Infirmary, Oxford, UK. Clin Endocrinol (Oxf). 2001 Jul;55(1):87-92. OBJECTIVE: Although growth hormone (GH) has well documented insulin antagonistic effects, GH deficient adults often demonstrate insulin resistance. In young GH deficient children, increased susceptibility to hypoglycaemia might indicate increased insulin sensitivity; however, this has not been documented. We therefore determined insulin sensitivity in GH deficient and GH sufficient children. DESIGN AND PATIENTS: Prospective study of children undergoing insulin tolerance tests for clinical investigation of GH or cortisol secretion at a regional Paediatric Endocrine/Growth Clinic between October 1986 and December 1997. Ninety-one tests were performed in children with GH deficiency and 142 tests in children with normal GH response to insulin (peak GH > or = 20 IU/l). MEASUREMENTS: The standard insulin tolerance test was modified to permit frequent measurements of glucose (0, 5, 10, 15, 20, 30, 45, 60 and 90 minutes). Rate of log glucose disappearance in the first 15 minutes was calculated as a direct measure of insulin sensitivity. RESULTS: GH deficient children were more insulin sensitive than GH sufficient children (P = 0.004) and had lower glucose nadirs post-insulin (P = 0.005). Subgroup analysis revealed that these differences were greater in younger (< 12 years old) or pre/early pubertal children. In 14 prepubertal children, exogenous sex steroid priming resulted in lower insulin sensitivity (P < 0.05) compared to nonprimed tests. CONCLUSIONS: Young GH deficient children were more insulin sensitive than children with normal GH secretion. Th Continue reading >>

More in diabetes