| Lack of dietary carbohydrates induces hepatic growth hormone (GH) resistance in rats. | |
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MedLine Citation:
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PMID: 21427215 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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GH is a well established regulator of growth, lipid, and glucose metabolism and therefore important for fuel utilization. However, little is known about the effects of macronutrients on the GH/IGF system. We used low-carbohydrate/high-fat diets (LC-HFD) as a model to study the impact of fat, protein, and carbohydrates on the GH/IGF-axis; 12-wk-old Wistar rats were fed either regular chow, a moderate, protein-matched LC-HFD, or a ketogenic LC-HFD (percentage of fat/protein/carbohydrates: chow, 16.7/19/64.3; LC-HF-1, 78.7/19.1/2.2; LC-HF-2, 92.8/5.5/1.7). After 4 wk, body and tibia length, lean body mass, and fat pad weights were measured. Furthermore, we investigated the effects of LC-HFD on 1) secretion of GH and GH-dependent factors, 2) expression and signaling of components of the GH/IGF system in liver and muscle, and 3) hypothalamic and pituitary regulation of GH release. Serum concentrations of IGF-I, IGF binding protein-1, and IGF binding protein-3 were lower with LC-HF-1 and LC-HF-2 (P < 0.01). Both LC-HFD-reduced hepatic GH receptor mRNA and protein expression, decreased basal levels of total and phosphorylated Janus kinase/signal transducers and activators of transcription signaling proteins and reduced hepatic IGF-I gene expression. Hypothalamic somatostatin expression was reduced only with LC-HF-1, leading to increased pituitary GH secretion, higher IGF-I gene expression, and activation of IGF-dependent signaling pathways in skeletal muscle. In contrast, despite severely reduced IGF-I concentrations, GH secretion did not increase with LC-HF-2 diet. In conclusion, lack of carbohydrates in LC-HFD induces hepatic GH resistance. Furthermore, central feedback mechanisms of the GH/IGF system are impaired with extreme, ketogenic LC-HFD. |
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Authors:
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Maximilian Bielohuby; Mandy Sawitzky; Barbara J M Stoehr; Peggy Stock; Dominik Menhofer; Sabine Ebensing; Mette Bjerre; Jan Frystyk; Gerhard Binder; Christian Strasburger; Zida Wu; Bruno Christ; Andreas Hoeflich; Martin Bidlingmaier |
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Publication Detail:
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Type: Journal Article Date: 2011-03-22 |
Journal Detail:
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Title: Endocrinology Volume: 152 ISSN: 1945-7170 ISO Abbreviation: Endocrinology Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-04-22 Completed Date: 2011-07-22 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: United States |
Other Details:
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Languages: eng Pagination: 1948-60 Citation Subset: AIM; IM |
Affiliation:
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Endocrine Research Unit, Medizinische Klinik-Innenstadt, Ludwig-Maximilians University, Munich, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blotting, Western Body Composition / drug effects Body Weight / drug effects Diet, Carbohydrate-Restricted* Dietary Carbohydrates / administration & dosage, pharmacology* Dietary Fats / administration & dosage, pharmacology Dietary Proteins / administration & dosage, pharmacology Gene Expression / drug effects Glycogen Synthase Kinase 3 / metabolism Growth Hormone / blood, genetics, metabolism* Insulin-Like Growth Factor Binding Proteins / blood, genetics, metabolism Insulin-Like Growth Factor I / genetics, metabolism Liver / drug effects*, metabolism Male Proto-Oncogene Proteins c-akt / metabolism Rats Rats, Wistar Receptors, Somatotropin / genetics, metabolism Reverse Transcriptase Polymerase Chain Reaction STAT3 Transcription Factor / metabolism STAT5 Transcription Factor / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Dietary Carbohydrates; 0/Dietary Fats; 0/Dietary Proteins; 0/Insulin-Like Growth Factor Binding Proteins; 0/Receptors, Somatotropin; 0/STAT3 Transcription Factor; 0/STAT5 Transcription Factor; 67763-96-6/Insulin-Like Growth Factor I; 9002-72-6/Growth Hormone; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/glycogen synthase kinase 3 beta; EC 2.7.11.26/Glycogen Synthase Kinase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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