diabetestalk.net

Growth Hormone Antagonizes Insulin

Effects Of Growth Hormone On Glucose Metabolism.

Effects Of Growth Hormone On Glucose Metabolism.

Abstract Growth hormone (GH) counteracts in general the effects of insulin on glucose and lipid metabolism, but shares protein anabolic properties with insulin. Under physiological circumstances GH does not affect total glucose turnover directly. There is however evidence that GH acutely decreases glucose oxidation (secondary to an increase in lipid oxidation) and suppresses muscle uptake of glucose, suggesting that GH redistributes glucose fluxes into a non-oxidative pathway, which could be a build up of glycogen depots through gluconeogenesis. Since GH secretion is inhibited in the fed state these actions are mainly important in the postprandial or fasting state. Under pathological conditions of GH excess (e.g. acromegaly, poorly controlled tp. 1 diabetes or high dose GH treatment) the diabetogenic actions of GH become apparent. In these patients increased endogenous glucose production, decreased muscle glucose uptake and rising blood glucose levels are observed. In patients with intact beta-cell function these changes are counterbalanced by hyperinsulinemia--such hyperinsulinemia may in the long term induce increased cardiovascular morbidity and mortality ('Reavens syndrome X'). When stimulated with insulin these patients exhibit insulin resistance at the liver, in adipose tissue and in muscle. Few elaborate studies on the effects of GH on glucose metabolism in GH deficient patients have been conducted. These patients are hypersensitive to the actions of insulin on glucose metabolism and there is some evidence that when GH initially is given to such patients in the GH deprived state, paradox insulin-like effects of GH may be observed. Whether this may relate to increased activity of insulin-like growth factors is unsettled. Continue reading >>

Predictors Of Insulin-like Growth Factor-i Responses To Growth Hormone Replacement In Young Adults With Growth Hormone Deficiency

Predictors Of Insulin-like Growth Factor-i Responses To Growth Hormone Replacement In Young Adults With Growth Hormone Deficiency

Predictors of Insulin-Like Growth Factor-I Responses to Growth Hormone Replacement in Young Adults with Growth Hormone Deficiency Thankamony A.a Capalbo D.a Jonsson P.J.d Simpson H.L.b Dunger D.B.a, c aDepartment of Paediatrics, University of Cambridge, bWolfson Diabetes and Endocrine Clinic, Institute of Metabolic Science, Cambridge University Hospitals Foundation Trust, and cNational Institute for Health Research (NIHR) Cambridge Comprehensive Biomedical Research Centre, Cambridge, UK; dKIMS Medical Outcomes, Pfizer Endocrine Care, Sollentuna, Sweden Background/Aims: Physiological growth hormone (GH) secretion and insulin-like growth factor-I (IGF-I) levels are greater in young compared to older adults. We evaluated IGF-I levels and predictors of IGF-I responses in young adults on GH replacement. Design: From the KIMS database, 310 young adults (age 15-26 years) with severe GH deficiency related to childhood-onset disease and commenced on adult GH replacement' were identified. IGF-I responses' were estimated from first-year increments in IGF-I standard deviation scores (SDS) and adjusted for GH dose. Body composition was assessed by bioimpedance in 143 patients. Results: IGF-I levels increased markedly from baseline to 1 year of replacement (-3.75 1.94 vs. -1.36 1.86 SDS, p < 0.0001), but remained low compared to normative data despite dose titration. In multivariate models, IGF-I responses were positively associated with age [B (SE) SDS/(mg/m2); 0.52 (0.15), p = 0.0007] and BMI SDS [1.06 (0.25), p < 0.0001] and inversely associated with female gender [-4.45 (0.79), p < 0.0001] and baseline IGF-I SDS [-1.44 (0.20), p < 0.0001]. IGF-I responses were positively associated with first-year increases in lean body mass (r = 0.19, p = 0.003) and haemoglobin A1c (r = 0.15, p Continue reading >>

An Evaluation Of Growth Hormone And Igf-1 Responses In Neonates With Hyperinsulinaemic Hypoglycaemia

An Evaluation Of Growth Hormone And Igf-1 Responses In Neonates With Hyperinsulinaemic Hypoglycaemia

An Evaluation of Growth Hormone and IGF-1 Responses in Neonates with Hyperinsulinaemic Hypoglycaemia Senthil Senniappan 1,2and Khalid Hussain 1,2 1Department of Paediatric Endocrinology, Great Ormond Street Hospital for Children, NHS Trust, WC1N 3JH, UK 2Developmental Endocrinology Research Group, Molecular Genetics Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK Received 25 February 2013; Revised 16 August 2013; Accepted 2 September 2013 Copyright 2013 Senthil Senniappan and Khalid Hussain. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Hyperinsulinaemic Hypoglycaemia (HH) is the most common cause of severe and persistent hypoglycemia in the neonatal period. It has been shown that the neonates with HH fail to generate adequate serum cortisol counterregulatory response to symptomatic hypoglycemia. However the role played by growth hormone (GH) and Insulin-like Growth Factor 1 (IGF-1) is not clear. Objectives. To compare the serum GH, IGF-1, and IGFBP3 responses to HH in neonates undergoing diagnostic fasting studies. Population and Methods. Data was retrospectively collected on full-term neonates who presented with severe and persistent hypoglycemia and were confirmed to have HH. Neonates born with intrauterine growth retardation or those on medical therapy (diazoxide or octreotide) were excluded. Results. 31 neonates with HH (mean gestational age: 38 weeks and mean birth weight: 3.9 kg) were included in the study. The mean age at the time of diagnostic fast was 4 weeks, the mean glucose concentration during the fast was 2.2 mmol/L ( ), and Continue reading >>

Counterregulatory Hormone

Counterregulatory Hormone

Dorit Koren*, Andrew Palladino**, in Genetic Diagnosis of Endocrine Disorders (Second Edition) , 2016 Hypoglycemia Due to Counterregulatory Hormone Deficiency The counterregulatory hormones glucagon, epinephrine, cortisol, and growth hormone act to stimulate key endogenous glucose production pathways, as discussed in the Introduction and outlined in Fig.3.1. Thus, deficiency of either the counterregulatory hormones or the factors that control these hormones production and secretion (e.g., ACTH deficiency) may also predispose to hypoglycemia. These deficiencies may be single or may be seen in combination, as in hypopituitarism. Genetic defects leading to counterregulatory hormone deficiency are discussed individually in the subsequent sections. Congenital Pituitary Hormone Deficiencies The anterior pituitary gland contains five different populations of cells, which produce six different hormones: somatotrophs, which produce GH; gonadotrophs, which produce luteinizing hormone (LH), and follicle stimulating hormone (FSH), which acts on the gonads to produce sex steroids; corticotrophs, which produce adrenocorticotropic hormone (ACTH), which acts on the adrenal glands to stimulate glucocorticoids and sex steroid production; thyrotrophs, which produce thyroid stimulating hormone (TSH), which act on the thyroid gland to stimulate thyroid hormone production; and lactotrophs, which produce prolactin. The anterior pituitary hormones that are involved in counterregulation and glucose homeostasis are GH, which itself is one of the counteregulatory hormones, and ACTH, which as aforementioned stimulates cortisol production. Hypoglycemia in the neonatal period is a common presenting feature of deficiencies of GH or ACTH in isolation or of multiple pituitary hormones. A large number Continue reading >>

Growth Hormone | Definition, Function, Deficiency, & Excess | Britannica.com

Growth Hormone | Definition, Function, Deficiency, & Excess | Britannica.com

Alternative Titles: GH, HGH, STH, human growth hormone, somatotropic hormone, somatotropin Growth hormone (GH), also called somatotropin or human growth hormone, peptide hormone secreted by the anterior lobe of the pituitary gland . It stimulates the growth of essentially all tissues of the body, including bone . GH is synthesized and secreted by anterior pituitary cells called somatotrophs, which release between one and two milligrams of the hormone each day. GH is vital for normal physical growth in children; its levels rise progressively during childhood and peak during the growth spurt that occurs in puberty . pituitary glandGrowth hormone is secreted by the anterior lobe of the pituitary gland and is vital for normal physical growth in children. In biochemical terms, GH stimulates protein synthesis and increases fat breakdown to provide the energy necessary for tissue growth. It also antagonizes (opposes) the action of insulin . GH may act directly on tissues, but much of its effect is mediated by stimulation of the liver and other tissues to produce and release insulin-like growth factors , primarily insulin-like growth factor 1 (IGF-1; formerly called somatomedin). The term insulin-like growth factor is derived from the ability of high concentrations of these factors to mimic the action of insulin, although their primary action is to stimulate growth. Serum IGF-1 concentrations increase progressively with age in children, with an accelerated increase at the time of the pubertal growth spurt. After puberty the concentrations of IGF-1 gradually decrease with age, as do GH concentrations. GH secretion is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by somatostatin . In addition, GH secretion is pulsatile, with surges in secretion occurring Continue reading >>

Effects Of Growth Hormone On Glucose, Lipid, And Protein Metabolism In Human Subjects

Effects Of Growth Hormone On Glucose, Lipid, And Protein Metabolism In Human Subjects

In evolutionary terms, GH and intracellular STAT 5 signaling is a very old regulatory system. Whereas insulin dominates periprandially, GH may be viewed as the primary anabolic hormone during stress and fasting. GH exerts anabolic effects directly and through stimulation of IGF-I, insulin, and free fatty acids (FFA). When subjects are well nourished, the GH-induced stimulation of IGF-I and insulin is important for anabolic storage and growth of lean body mass (LBM), adipose tissue, and glycogen reserves. During fasting and other catabolic states, GH predominantly stimulates the release and oxidation of FFA, which leads to decreased glucose and protein oxidation and preservation of LBM and glycogen stores. The most prominent metabolic effect of GH is a marked increase in lipolysis and FFA levels. In the basal state, the effects of GH on protein metabolism are modest and include increased protein synthesis and decreased breakdown at the whole body level and in muscle together with decreased amino acid degradation/oxidation and decreased hepatic urea formation. During fasting and stress, the effects of GH on protein metabolism become more pronounced; lack of GH during fasting increases protein loss and urea production rates by approximately 50%, with a similar increase in muscle protein breakdown. GH is a counterregulatory hormone that antagonizes the hepatic and peripheral effects of insulin on glucose metabolism via mechanisms involving the concomitant increase in FFA flux and uptake. This ability of GH to induce insulin resistance is significant for the defense against hypoglycemia, for the development of “stress” diabetes during fasting and inflammatory illness, and perhaps for the “Dawn” phenomenon (the increase in insulin requirements in the early morning hou Continue reading >>

Welcome To Medfitness

Welcome To Medfitness

Growth hormone supplementation has been widely publicized lately due to recent allegations against Jason Grimsley and David Segui of Major League Baseball fame. People choose to take the supplement for a promise of augmented athletic performance or to turn back the clock on life, without chance of detection by governing agencies. Before jumping on the bandwagon, you should know what growth hormone is and what its effects are. The polypeptide human growth hormone, hGH, is one of the most important naturally occurring hormones for normal growth to adult size. It is normally secreted in a pulsatile fashion 6-12 times per day1, meaning concentrations fluctuate throughout the day. Growth hormone secretion peaks during puberty and decreases with age. Secretion is increased by sleep, stress, starvation, puberty, exercise, hypoglycemia (low blood sugar), and other hormones (ie growth hormone releasing hormone). hGH secretion is inhibited by somatostatin (from the hypothalamus), somatomedins (hormones released by the hGH target organs in response to a rise in hGH), obesity, hyperglycemia (high blood sugar) and pregnancy. It is important to understand that like many other hormone systems in the body, hGH and GHRH inhibit their own secretion as part of a negative feedback system. hGH is taken up by skeletal muscle6 and has many effects. It acts directly to decrease glucose uptake into cells, increase hepatic gluconeogenisis10, increase lipolysis (fat release from adipose cells)11, increase protein synthesis in muscle cells7,8,9, increase lean body mass and increase release of insulin like growth factor (IGF-1) from the liver and locally in skeletal muscle. IGF-1 increases bone length in children, increases protein synthesis in muscle and increases lean body mass. Both growth horm Continue reading >>

Endocrine Function Flashcards | Quizlet

Endocrine Function Flashcards | Quizlet

interacting w/ target cells on glands and tissues located at the base of the brain; "master gland"; divided into posterior and anterior secretes TSH, growth hormone, adrenocorticotropic hormone (ACTH), follicle-stimulating hormone, luteinizing hormone, prolactin melanocyte-stimulating hormone, antidiuretic hormone, & oxytocin basal portion of diencephalon; regulates pituitary gland; connects nervous and endocrine systems; contains receptors that monitor hormone, nutrient and ion levels that stimulate the hypothalamus to secrete releasing and inhibiting hormones; hypothalamus regulates hormones produced by anterior pituitary and brain controls posterior pituitary gland organ with exocrine and endocrine functions; lies under the stomach b/t the kidneys in the retroperitoneum; endocrine functions are carried out by the approx 1 million islets of Langerhans, situated among the many small acini (cell clusters that produce digestive enzymes) -Alpha cells secrete glucagon when serum glucose levels fall -Beta cells secrete insulin when serum glucose increase and amylin to enhance insulin -Delta cells secrete somatostatin, which regulates insulin and glucagon -PP cells secrete pancreatic polypeptide, which regulates some other pancreatic activities -Epsilon cells secrete ghrelin, which stimulates hunger works with liver to maintain blood sugar levels; liver controls glucose and pancreas controls insulin efficient fuel used by brain and nervous system; enters GI tract then travels portal vein to liver, liver sends it to circulatory system, tissue then retrieves it from blood -synthesis for glucose from noncarbohydrate source (amino acids, lactic acid, triglycerides) most efficient form of fuel storage; all cells except bran and RBCs use it; initial breakdown occurs in liver; it Continue reading >>

Blood Sugar Regulation

Blood Sugar Regulation

Ball-and-stick model of a glucose molecule Blood sugar regulation is the process by which the levels of blood sugar, primarily glucose, are maintained by the body within a narrow range. This tight regulation is referred to as glucose homeostasis. Insulin, which lowers blood sugar, and glucagon, which raises it, are the most well known of the hormones involved, but more recent discoveries of other glucoregulatory hormones have expanded the understanding of this process.[1] Mechanisms[edit] Blood sugar regulation the flatline is the level needed the sine wave the fluctuations. Blood sugar levels are regulated by negative feedback in order to keep the body in balance. The levels of glucose in the blood are monitored by many tissues, but the cells in the pancreatic islets are among the most well understood and important. Glucagon[edit] If the blood glucose level falls to dangerous levels (as during very heavy exercise or lack of food for extended periods), the alpha cells of the pancreas release glucagon, a hormone whose effects on liver cells act to increase blood glucose levels. They convert glycogen into glucose (this process is called glycogenolysis). The glucose is released into the bloodstream, increasing blood sugar. Hypoglycemia, the state of having low blood sugar, is treated by restoring the blood glucose level to normal by the ingestion or administration of dextrose or carbohydrate foods. It is often self-diagnosed and self-medicated orally by the ingestion of balanced meals. In more severe circumstances, it is treated by injection or infusion of glucagon. Insulin[edit] When levels of blood sugar rise, whether as a result of glycogen conversion, or from digestion of a meal, a different hormone is released from beta cells found in the Islets of Langerhans in the p 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 Shin-Hye Kim , MD, PhD and Mi-Jung Park , MD, PhD 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 2017 Aug 31; Accepted 2017 Sep 11. Copyright 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, muscle, fat, and kidney [ 1 ]. Insulin, the primary regulator of glucose balance, lowers postprandial plasma glucos Continue reading >>

Human Growth Hormone And Insulin Are Friends

Human Growth Hormone And Insulin Are Friends

High-level nutrition coaching - 2 Week FREE Trial. Get your custom plan & start losing fat with our NEW Fat Loss Trends app! Human Growth Hormone and Insulin are Friends Hormone balance, and the cycle by which our hormones are regulated, is very complicated. Thats why we have doctors who specialize in endocrinology. This article is intended as a basic explanation of the function of a few hormones and their interactions within the human body, as well as how nutrition/exercise affect their production and utilization. That said, hormone manipulation through diet and exercise does NOT account for a great deal of your results you should focus on getting better at exercise, eating enough, and recovering properly before you lose sleep over whether or not you have optimal HGH or insulin levels. Ill get down to brass tacks and make myself clear: insulin and growth hormone play antagonist roles against one another. When one is elevated, the other will be low. That does not, however, mean that their functions are all that dissimilar; theyre both responsible for growth in different ways and looking at them as synergists is much more productive. We want to find a way to make the best of insulins ability to pull nutrients into cells, but we also want to elicit the muscular, skeletal and neurological growth that (as the name implies) growth hormone is responsible for. Intraday nutrient cycling is the best way to do this. Understanding why is complicated as all heck, but weve tried to make it easy to digest (Get it? Digest? Haha?) Before we continue, I am going to ask that you take a look at our articles on insulin and leptin , as well as the sleep tutorial . Theyll help you understand some of the terms in this section and get a better idea of whats really going on behind the scenes. Continue reading >>

Adult Growth Hormone Deficiency

Adult Growth Hormone Deficiency

Human Growth Foundation depends on our members and donors like you. Please click on a choice below and visit our donations page. Principal Source of Information for Adult Growth Hormone Deficiency Nature and Physiology of Growth Hormone (top) Growth hormone is a major body system-wide metabolic hormone that regulates protein, lipid (fat), and carbohydrate homeostasis (balance). In addition to being an anabolic hormone, it also has fat mobilizing diabetogenic properties (i.e., can cause a rise in blood glucose levels). The body produces several kinds of growth hormone. The principal form of growth hormone in humans is a complex protein that weighs 22 kd (kilodaltons) and contains 191 amino acids. It is known as somatotrope; and, what is usually reference when discussing growth horomone (GH). GH is produced by growth hormone cells, known as somatotropes, which are located in the anterior lobe of the pituitary located in the brain. The GH somatotrope cells secrete approximately 50% of the hormone-producing cells of the anterior pituitary. Growth hormone (GH) is required for growth, development, and maintenance of the body and mind of humans and many other forms of life from conception through the end of life. The hypothalamus gland is located in the brain just above the pituitary. The pituitary branches into two lobes; and, is connected to the hypothalamus by a pituitary stalk. The pituitary stalk is the pathway through which the hypothalamus transmits neuroendocrine signals or messages to the pituitary. In turn, the pituitary mediates or regulates the production of numerous hormones by various glands. The hypothalamic neuroendocrine messenger that directs the anterior lobe of the pituitary to produce GH is called growth hormone releasing hormone (GHRH). GH is mediated or Continue reading >>

Growth Hormone Stimulates Skeletal Muscle Protein Synthesis And Antagonizesinsulin's Antiproteolytic Action In Humans.

Growth Hormone Stimulates Skeletal Muscle Protein Synthesis And Antagonizesinsulin's Antiproteolytic Action In Humans.

Growth hormone stimulates skeletal muscle protein synthesis and antagonizesinsulin's antiproteolytic action in humans. Fryburg DA(1), Louard RJ, Gerow KE, Gelfand RA, Barrett EJ. (1)Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut. We examined the effects of a combined, local intra-arterial infusion of growthhormone (GH) and insulin on forearm glucose and protein metabolism in sevennormal adults. GH was infused into the brachial artery for 6 h with a dose that, in a previous study, stimulated muscle protein synthesis (phenylalanine Rd)without affecting systemic GH, insulin, or insulinlike growth factor Iconcentrations. For the last 3 h of the GH infusion, insulin was coinfused with adose that, in the absence of infused GH, suppressed forearm muscle proteolysis by30-40% without affecting systemic insulin levels. Measurements of forearmglucose, amino acid balance, and [3H]phenylalanine and [14C]leucine kinetics weremade at 3 and 6 h of the infusion. Glucose uptake by forearm tissues in response to GH and insulin did not change significantly between 3 and 6 h. By 6 h, thecombined infusion of GH and insulin promoted a significantly more positive netbalance of phenylalanine, leucine, isoleucine, and valine (all P less than 0.05).The change in net phenylalanine balance was due to a significant increase inphenylalanine Rd (51%, P less than 0.05) with no observable change inphenylalanine Ra. For leucine, a stimulation of leucine Rd (50%, P less than0.05) also accounted for the change in leucine net balance, with no suppressionof leucine Ra. The stimulation of Rd, in the absence of an observed effect on Ra,suggests that GH blunts the action of insulin to suppress proteolysis in additionto blunting insulin's action on Rd. Continue reading >>

Counterregulatory Hormones

Counterregulatory Hormones

Hormones that work against the action of insulin, raising blood glucose levels in response to hypoglycemia (low blood sugar). The main counterregulatory hormones are glucagon, epinephrine (also known as adrenaline), cortisol, and growth hormone. People who don’t have diabetes have a number of defense mechanisms against hypoglycemia. First, the pancreas decreases its insulin output, allowing blood glucose to rise. Second, the alpha cells of the pancreas secrete the counterregulatory hormone glucagon, which signals the liver to release more glucose. Third, the adrenal glands secrete epinephrine, which signals the liver and kidneys to produce more glucose; in addition, epinephrine keeps certain body tissues, such as muscle, from using as much glucose from the bloodstream, and it acts to reduce insulin secretion. Epinephrine is the same “fight or flight” hormone that revs the body up in response to danger, and it produces the symptoms that normally herald an episode of hypoglycemia, such as hunger, sweating, trembling, “butterflies,” and heart palpitations. In some cases, especially when glucagon and epinephrine fail to adequately raise blood glucose levels, the body releases cortisol and growth hormone, which can also increase blood glucose levels. After years of having Type 1 diabetes, many individuals lose most of these defenses against hypoglycemia. To begin with, they are not able to benefit from reduced secretion of insulin by the pancreas; the reason why people with Type 1 diabetes must use injected or infused insulin is that the pancreas no longer makes insulin at all. Also, for reasons unknown, people with Type 1 diabetes usually lose their ability to secrete glucagon. In addition, after recurring episodes of even mild hypoglycemia, the epinephrine respon Continue reading >>

Jci -effects Of Physiologic Levels Of Glucagon And Growth Hormone On Human Carbohydrate And Lipid Metabolism. Studies Involving Administration Of Exogenous Hormone During Suppression Of Endogenous Hormone Secretion With Somatostatin.

Jci -effects Of Physiologic Levels Of Glucagon And Growth Hormone On Human Carbohydrate And Lipid Metabolism. Studies Involving Administration Of Exogenous Hormone During Suppression Of Endogenous Hormone Secretion With Somatostatin.

Effects of physiologic levels of glucagon and growth hormone on human carbohydrate and lipid metabolism. Studies involving administration of exogenous hormone during suppression of endogenous hormone secretion with somatostatin. J Clin Invest. 1976; 57(4) :875-884. . To study the individual effects of glucagon and growth hormone on human carbohydrate and lipid metabolism, endogenous secretion of both hormones was simultaneously suppressed with somatostatin and physiologic circulating levels of one or the other hormone were reproduced by exogenous infusion. The interaction of these hormones with insulin was evaluated by performing these studies in juvenile-onset, insulin-deficient diabetic subjects both during infusion of insulin and after its withdrawal. Infusion of glucagon (1 ng/kg-min) during suppression of its endogenous secretion with somatostatin produced circulating hormone levels of approximately 200 pg/ml. When glucagon was infused along with insulin, plasma glucose levels rose from 94 +/- 8 to 126 +/- 12 mg/100 ml over 1 h (P less than 0.01); growth hormone, beta-hydroxy-butyrate, alanine, FFA, and glycerol levels did not change. When insulin was withdrawn, plasma glucose, beta-hydroxybutyrate, FFA, and glycerol all rose to higher levels (P less than 0.01) than those observed under similar conditions when somatostatin alone had been infused to suppress glucagon secretion. Thus, under appropriate conditions, physiologic levels of glucagon can stimulate lipolysis and cause hyperketonemia and hyperglycemia in man; insulin antagonizes the lipolytic and ketogenic effects of glucagon more effectively than the hyperglycemic effect. Infusion of growth hormone (1 mug/kg-h) during suppression of its endogenous secretion with somastostatin produced circulating hormone l Continue reading >>

More in diabetes