scholarly journals A növekedési hormon és az inzulinszerű növekedési faktorok élettani szerepe

2019 ◽  
Vol 160 (45) ◽  
pp. 1774-1783 ◽  
Author(s):  
Tamás Halmos ◽  
Ilona Suba
Keyword(s):  
Growth Factors ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Free Fatty Acid ◽  
Tissue Growth ◽  
Acid Oxidation ◽  
Glucose Output ◽  
The Brain ◽  
Stimulation Of

Abstract: The existence of insulin-like growth factors (IGFs) was recognized in connection with the stimulation of sulfate incorporation into cartilage. IGFs take part in the embryonal development and postnatal growth, in interaction with the growth hormone (GH). The physiological effects of IGF1 are promotion of tissue growth and development, stimulation of cell proliferation, effects on lipid and carbohydrate metabolism, anti-aging, anti-inflammatory, anabolic, anti-oxidant, neuro- and hepatoprotective properties. Our knowledge about the GH/IGF axis is diverse, partly contradictory, their research is continued intensively nowadays. We considered it worthwhile to review and interpret this information. Study on GH/IGF medical reports, with particular reference to the less known metabolic control. 75% of the growth factors are produced in the liver by GH and insulin stimulation; their effects are expressed on specific receptors, and modified by specific binding proteins. IGF1 directly increases the muscle mass, bone density, and the structure of the bones. Intestinal microbiota induces secretion of IGF1, which promotes the development and remodeling of the bones. Short-chain fatty acids, produced in microbial fermented fibers, induce secretion of IGF1, suggesting that microbial activity also affects bone health via IGF1. IGF1 also has a direct and indirect glucose-lowering effect, enhances free fatty acid oxidation in the muscle, reducing the flow of free fatty acid into the liver, improving insulin signaling, resulting in the reduction of hepatic glucose output, and improves insulin sensitivity. IGF1 directly influences the expression of circadian BMAL1 in hypothalamic cells: this refers to the newly recognized ’zeitgeber’ role of IGF1. The bioactivity of insulin-like peptides in the brain is characterized by neuronal survival, excitatory and inhibitory neurotransmission, maintenance of normal free fatty acid levels, improvement of cognitive function, protection against cell damage, neurogenesis and angiogenesis. The effects of IGF2 are less outlined, however, it has a relevant role in the development of the fetus, and acts protectively on the brain. Lack or over-expression of IGF1 can be detected or may causally associated in many pathological conditions. According to these collected data, insulin sensitivity may be improved by different pathways. The role of IGFs in these processes should be a task of future research. Orv Hetil. 2019; 160(45): 1774–1783.

scholarly journals Nonoxidative Free Fatty Acid Disposal Is Greater in Young Women than Men

2011 ◽  
Vol 96 (2) ◽  
pp. 541-547 ◽  
Author(s):  
Christina Koutsari ◽  
Rita Basu ◽  
Robert A. Rizza ◽  
K. Sreekumaran Nair ◽  
Sundeep Khosla ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Free Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Specific Interaction ◽  
Serum Triglyceride ◽  
Nitrogen Excretion ◽  
Whole Body ◽  
Acid Oxidation ◽  
Peripheral Insulin Sensitivity

abstract Context: Large increases in systemic free fatty acid (FFA) availability in the absence of a corresponding increase in fatty acid oxidation can create a host of metabolic abnormalities. These adverse responses are thought to be the result of fatty acids being shunted into hepatic very low-density lipoprotein-triglyceride production and/or intracellular lipid storage and signaling pathways because tissues are forced to increase nonoxidative FFA disposal. Objective: The objective of the study was to examine whether variations in postabsorptive nonoxidative FFA disposal within the usual range predict insulin resistance and hypertriglyceridemia. Design: We measured: systemic FFA turnover using a continuous iv infusion of [9–10, 3H]palmitate; substrate oxidation with indirect calorimetry combined with urinary nitrogen excretion; whole-body and peripheral insulin sensitivity with the labeled iv glucose tolerance test minimal model. Setting: the study was conducted at the Mayo Clinic General Clinical Research Center. Participants: Participants included healthy, postabsorptive, nonobese adults (21 women and 21 men). Interventions: There were no interventions. Main Outcome Measures: Nonoxidative FFA disposal (micromoles per minute), defined as the FFA disappearance rate minus fatty acid oxidation. Results: Women had 64% greater nonoxidative FFA disposal rate than men but a better lipid profile and similar insulin sensitivity. There was no significant correlation between nonoxidative FFA disposal and whole-body sensitivity, peripheral insulin sensitivity, or fasting serum triglyceride concentrations in men or women. Conclusions: Healthy nonobese women have greater rates of nonoxidative FFA disposal than men, but this does not appear to relate to adverse health consequences. Understanding the sex-specific interaction between adipose tissue lipolysis and peripheral FFA removal will help to discover new approaches to treat FFA-induced abnormalities.

Free fatty acid as a link in the regulation of hepatic glucose output by peripheral insulin

Diabetes ◽  
1995 ◽  
Vol 44 (9) ◽  
pp. 1038-1045 ◽  
Author(s):  
K. Rebrin ◽  
G. M. Steil ◽  
L. Getty ◽  
R. N. Bergman
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output

scholarly journals Serum Amyloid Beta42 Is Not Eliminated by the Cirrhotic Liver: A Pilot Study

2021 ◽  
Vol 10 (12) ◽  
pp. 2669
Author(s):  
Reiner Wiest ◽  
Thomas S. Weiss ◽  
Lusine Danielyan ◽  
Christa Buechler
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Clearance ◽  
Protective Role ◽  
Tissue Growth ◽  
Cirrhotic Liver ◽  
Diabetic Patients ◽  
Peripheral Clearance ◽  
End Stage ◽  
The Brain

Amyloid-beta (Aβ) deposition in the brain is the main pathological hallmark of Alzheimer disease. Peripheral clearance of Aβ may possibly also lower brain levels. Recent evidence suggested that hepatic clearance of Aβ42 is impaired in liver cirrhosis. To further test this hypothesis, serum Aβ42 was measured by ELISA in portal venous serum (PVS), systemic venous serum (SVS), and hepatic venous serum (HVS) of 20 patients with liver cirrhosis. Mean Aβ42 level was 24.7 ± 20.4 pg/mL in PVS, 21.2 ± 16.7 pg/mL in HVS, and 19.2 ± 11.7 pg/mL in SVS. Similar levels in the three blood compartments suggested that the cirrhotic liver does not clear Aβ42. Aβ42 was neither associated with the model of end-stage liver disease score nor the Child–Pugh score. Patients with abnormal creatinine or bilirubin levels or prolonged prothrombin time did not display higher Aβ42 levels. Patients with massive ascites and patients with large varices had serum Aβ42 levels similar to patients without these complications. Serum Aβ42 was negatively associated with connective tissue growth factor levels (r = −0.580, p = 0.007) and a protective role of Aβ42 in fibrogenesis was already described. Diabetic patients with liver cirrhosis had higher Aβ42 levels (p = 0.069 for PVS, p = 0.047 for HVS and p = 0.181 for SVS), which is in accordance with previous reports. Present analysis showed that the cirrhotic liver does not eliminate Aβ42. Further studies are needed to explore the association of liver cirrhosis, Aβ42 levels, and cognitive dysfunction.

scholarly journals Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

2021 ◽  
Vol 22 (11) ◽  
pp. 6071
Author(s):  
Suzanne Gascon ◽  
Jessica Jann ◽  
Chloé Langlois-Blais ◽  
Mélanie Plourde ◽  
Christine Lavoie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factors ◽  
Signaling Pathways ◽  
Brain Structures ◽  
Therapeutic Strategies ◽  
Native Proteins ◽  
Receptor Sites ◽  
The Brain

Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations.

ChemInform Abstract: Role of Heart-Type Fatty Acid Binding Protein in the Brain Function

ChemInform ◽  
2009 ◽  
Vol 40 (26) ◽  
Author(s):  
Keiju Motohashi ◽  
Yui Yamamoto ◽  
Norifumi Shioda ◽  
Hisatake Kondo ◽  
Yuji Owada ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Brain Function ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
The Brain

scholarly journals Stimulation of Mitochondrial Fatty Acid Oxidation by Growth Hormone in Human Fibroblasts1

1997 ◽  
Vol 82 (12) ◽  
pp. 4208-4213 ◽  
Author(s):  
Kin-Chuen Leung ◽  
Ken K. Y. Ho
Keyword(s):  
Fatty Acid ◽  
Growth Factor ◽  
Lipid Oxidation ◽  
Palmitic Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I ◽  
Stimulation Of

In vivo administration of GH induces lipolysis and lipid oxidation. However, it is not clear whether the stimulation of lipid oxidation is a direct effect of GH or is driven by increased substrate supply secondary to lipolysis. An in vitro bioassay has been established for assessing β-oxidation of fatty acids in mitochondria, based on the measurement of conversion of tritiated palmitic acid to 3H2O by fibroblasts in culture. We have modified this assay to investigate whether GH stimulates fatty acid oxidation. GH stimulated oxidation of palmitic acid maximally by 26.7 ± 2.5% (mean ± sem; P < 0.0001). The stimulation was biphasic, with the oxidation rate increasing with increasing GH concentration to a peak response at 1.5 nmol/L and declining to a level not significantly different from control thereafter. Insulin-like growth factor-I at concentrations of up to 250 nmol/L had no significant effect on fatty acid oxidation. GH-binding protein attenuated the effect of GH. An anti-GH receptor (GHR) antibody (MAb263), which dimerizes the receptor and induces GH-like biological actions, significantly stimulated fatty acid oxidation. Another anti-GHR antibody (MAb5), which prevents receptor dimerization, suppressed GH action. In summary, GH directly stimulated fatty acid oxidation, an action not mediated by insulin-like growth factor-I. Dimerization of GHRs was necessary for this effect. This bioassay is a practical tool for studying the regulatory effects of GH on lipid oxidation.

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