Biomaterial Database

Metabolic consequences of recombinant human growth hormone therapy in patients with Turner syndrome. 2023

Maria Gnacińska, and Hanna Magnuszewska, and Krzysztof Sworczak

Department of Endocrinology and Internal Medicine, Medical University of Gdansk, Poland.

BACKGROUND Turner syndrome (TS) predisposes to metabolic complications. Currently, TS patients are treated with recombinant human growth hormone (rGH) as standard therapy. The long-term effect of this therapy on carbohydrate metabolism remains unclear. Aim of the study: To assess possible metabolic alterations following rGH therapy. METHODS Material and methods: We enrolled 53 TS participants, comprising 37 patients who finished rGH therapy (group 1) and 16 patients who did not receive growth promoting therapy (group 2). Several anthropometric measurements were made. Carbohydrate and lipid metabolism, adipokines, and hs-CRP were assessed basing on laboratory test. The following indices were calculated: HOMA-IR, HOMA-b, QUICKI, and Matsuda. RESULTS There were no statistically significant differences between the 2 groups in terms of BMI or WHR. There was a statistically significant lower mean percentage of fat tissue in group 1 compared to group 2 (27.46% vs. 31.75%). Insulin resistance and sensitivity indices were not statistically different between groups. Using the Matsuda index, more patients who met criteria of insulin resistance were found in group 2 than in group 1 (56.25% vs. 37.84%); however, this difference was not statistically significant (p = 0.2). No statistically significant differences were found in lipid profile, adipokines, and hsCRP between groups. CONCLUSIONS rGH therapy leads to a beneficial change in body composition of TS patients despite unchanged BMI. A decrease in body fat persists for several years after finishing rGH treatment; rGH treatment is connected with a trend toward increased insulin sensitivity.

UI	MeSH Term	Description	Entries
D007328	Insulin	A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).	Iletin,Insulin A Chain,Insulin B Chain,Insulin, Regular,Novolin,Sodium Insulin,Soluble Insulin,Chain, Insulin B,Insulin, Sodium,Insulin, Soluble,Regular Insulin
D007333	Insulin Resistance	Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.	Insulin Sensitivity,Resistance, Insulin,Sensitivity, Insulin
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D014424	Turner Syndrome	A syndrome of defective gonadal development in phenotypic females associated with the karyotype 45,X (or 45,XO). Patients generally are of short stature with undifferentiated GONADS (streak gonads), SEXUAL INFANTILISM, HYPOGONADISM, webbing of the neck, cubitus valgus, elevated GONADOTROPINS, decreased ESTRADIOL level in blood, and CONGENITAL HEART DEFECTS. NOONAN SYNDROME (also called Pseudo-Turner Syndrome and Male Turner Syndrome) resembles this disorder; however, it occurs in males and females with a normal karyotype and is inherited as an autosomal dominant.	Bonnevie-Ullrich Syndrome,Gonadal Dysgenesis, 45,X,Gonadal Dysgenesis, XO,Monosomy X,Status Bonnevie-Ullrich,Turner's Syndrome,Ullrich-Turner Syndrome,Bonnevie Ullrich Syndrome,Status Bonnevie Ullrich,Syndrome, Ullrich-Turner,Turners Syndrome,Ullrich Turner Syndrome,XO Gonadal Dysgenesis
D054392	Adipokines	Polypeptides produced by the ADIPOCYTES. They include LEPTIN; ADIPONECTIN; RESISTIN; and many cytokines of the immune system, such as TUMOR NECROSIS FACTOR-ALPHA; INTERLEUKIN-6; and COMPLEMENT FACTOR D (also known as ADIPSIN). They have potent autocrine, paracrine, and endocrine functions.	Adipocytokine,Adipocytokines,Adipokine
D019382	Human Growth Hormone	A 191-amino acid polypeptide hormone secreted by the human adenohypophysis (PITUITARY GLAND, ANTERIOR), also known as GH or somatotropin. Synthetic growth hormone, termed somatropin, has replaced the natural form in therapeutic usage such as treatment of dwarfism in children with growth hormone deficiency.	Somatotropin (Human),Somatropin (Human),Cryo-Tropin,Genotonorm,Genotropin,Humatrope,Maxomat,Norditropin,Norditropin Simplexx,Norditropine,Nutropin,Omnitrope,Recombinant Human Growth Hormone (Mammalian),Saizen,Serostim,Somatropin,Umatrope,Zomacton,hGH (Human Growth Hormone),r-hGH(m),r-hGH-M,Cryo Tropin,CryoTropin,Growth Hormone, Human
D024821	Metabolic Syndrome	A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome include ABDOMINAL OBESITY; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state.	Cardiometabolic Syndrome,Insulin Resistance Syndrome X,Metabolic Syndrome X,Reaven Syndrome X,Dysmetabolic Syndrome X,Metabolic Cardiovascular Syndrome,Metabolic X Syndrome,Syndrome X, Insulin Resistance,Syndrome X, Metabolic,Cardiometabolic Syndromes,Cardiovascular Syndrome, Metabolic,Cardiovascular Syndromes, Metabolic,Metabolic Syndromes,Syndrome X, Dysmetabolic,Syndrome X, Reaven,Syndrome, Cardiometabolic,Syndrome, Metabolic,Syndrome, Metabolic Cardiovascular,Syndrome, Metabolic X,Syndromes, Cardiometabolic,Syndromes, Metabolic,X Syndrome, Metabolic