Dual effects of fructose on ChREBP and FoxO1/3α are responsible for AldoB up-regulation and vascular remodelling

2017 ◽  
Vol 131 (4) ◽  
pp. 309-325 ◽  
Author(s):  
Wei Cao ◽  
Tuanjie Chang ◽  
Xiao-qiang Li ◽  
Rui Wang ◽  
Lingyun Wu
Keyword(s):  
Structural Changes ◽  
Serum Levels ◽  
Pcr Analysis ◽  
Diabetic Patients ◽  
Vascular Remodelling ◽  
Vessel Wall Thickness ◽  
Vsmc Proliferation ◽  
Normal Glucose Level ◽  
Aldolase B ◽  
Underlying Mechanisms

Increased production of methylglyoxal (MG) in vascular tissues is one of the causative factors for vascular remodelling in different subtypes of metabolic syndrome, including hypertension and insulin resistance. Fructose-induced up-regulation of aldolase B (AldoB) contributes to increased vascular MG production but the underlying mechanisms are unclear. Serum levels of MG and fructose were determined in diabetic patients with hypertension. MG level had significant positive correlations with blood pressure and fructose level respectively. C57BL/6 mice were fed with control or fructose-enriched diet for 3 months and ultrasonographic and histologic analyses were performed to evaluate arterial structural changes. Fructose-fed mice exhibited hypertension and high levels of serum MG with normal glucose level. Fructose intake increased blood vessel wall thickness and vascular smooth muscle cell (VSMC) proliferation. Western blotting and real-time PCR analysis revealed that AldoB level was significantly increased in both the aorta of fructose-fed mice and the fructose-treated VSMCs, whereas aldolase A (AldoA) expression was not changed. The knockdown of AldoB expression prevented fructose-induced MG overproduction and VSMC proliferation. Moreover, fructose significantly increased carbohydrate-responsive element-binding protein (ChREBP), phosphorylated FoxO1/3α and Akt1 levels. Fructose induced translocation of ChREBP from the cytosol to nucleus and activated AldoB gene expression, which was inhibited by the knockdown of ChREBP. Meanwhile, fructose caused FoxO1/3α shuttling from the nucleus to cytosol and inhibited its binding to AldoB promoter region. Fructose-induced AldoB up-regulation was suppressed by Akt1 inhibitor but enhanced by FoxO1/3α siRNA. Collectively, fructose activates ChREBP and inactivates FoxO1/3α pathways to up-regulate AldoB expression and MG production, leading to vascular remodelling.

Role of Inflammatory Markers in Elderly Type 2 Diabetic Patients with Mild Cognitive Impairment

2019 ◽  
Vol 15 (3) ◽  
pp. 247-253 ◽  
Author(s):  
Salwa S. Hosny ◽  
Ahmed M. Bahaaeldin ◽  
Mohamed S. Khater ◽  
Meram M. Bekhet ◽  
Hayam A. Hebah ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Elderly Patients ◽  
Vascular Disease ◽  
Plasma Glucose ◽  
Serum Levels ◽  
Diabetic Patients ◽  
Hs Crp ◽  
And Control

<P>Background: Type 2 diabetes (T2DM) is a risk factor for Alzheimer’s disease and mild cognitive impairment. The etiology of cognitive impairment in people with T2DM is uncertain but, chronic hyperglycemia, cerebral micro vascular disease, severe hypoglycemia, and increased prevalence of macro vascular disease are implicated. </P><P> Objectives: To determine the serum levels of soluble vascular adhesion molecule (sVCAM-1) and highly sensitive C-reactive protein (hs-CRP) in elderly type 2 diabetics with mild cognitive impairment (MCI). Methods: Our study was conducted on 90 elderly subjects (aged 60 years old or more). They were divided into Group І, 30 patients with T2DM and mild cognitive impairment, group ІІ, 30 patients with T2DM without cognitive impairment and group III, 30 healthy subjects as a control group. They were subjected to history taking, full clinical examination, anthropometric measurement, the Addenbrooke’s Cognitive Examination III (ACE---III 2012), Fasting plasma glucose, 2 hours plasma glucose, HbA1c, lipid profile, protein/creatinine ratio, serum sVCAM-1 and hs-CRP. Results: Serum levels of sVCAM-1 in diabetic elderly patients with MCI were significantly higher (946.7 ± 162.01 ng/ml) than diabetic elderly patients without cognitive impairment (479.06 ± 65.27 ng/ml) and control (263.7 ± 72.05 ng/ml) with (P=0.002). Serum levels of Hs-CRP in diabetic elderly patients with MCI were significantly higher than as diabetic elderly patients without cognitive impairment and control with (P=0.005). Conclusion: Elderly diabetic patients with mild cognitive impairment have higher levels of soluble adhesion molecules and markers of low-grade systemic inflammation than other groups.</P>

scholarly journals IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1686
Author(s):  
Adelaida M. Celaya ◽  
Lourdes Rodríguez-de la Rosa ◽  
Jose M. Bermúdez-Muñoz ◽  
José M. Zubeldia ◽  
Carlos Romá-Mateo ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inflammatory Cytokines ◽  
Noise Exposure ◽  
Sensorineural Deafness ◽  
Serum Levels ◽  
Genetic Syndromes ◽  
Expression Ratio ◽  
Postnatal Maturation ◽  
Age Related ◽  
Underlying Mechanisms

Insulin-like growth factor 1 (IGF-1) deficiency is an ultrarare syndromic human sensorineural deafness. Accordingly, IGF-1 is essential for the postnatal maturation of the cochlea and the correct wiring of hearing in mice. Less severe decreases in human IGF-1 levels have been associated with other hearing loss rare genetic syndromes, as well as with age-related hearing loss (ARHL). However, the underlying mechanisms linking IGF-1 haploinsufficiency with auditory pathology and ARHL have not been studied. Igf1-heterozygous mice express less Igf1 transcription and have 40% lower IGF-1 serum levels than wild-type mice. Along with ageing, IGF-1 levels decreased concomitantly with the increased expression of inflammatory cytokines, Tgfb1 and Il1b, but there was no associated hearing loss. However, noise exposure of these mice caused increased injury to sensory hair cells and irreversible hearing loss. Concomitantly, there was a significant alteration in the expression ratio of pro- and anti-inflammatory cytokines in Igf1+/− mice. Unbalanced inflammation led to the activation of the stress kinase JNK and the failure to activate AKT. Our data show that IGF-1 haploinsufficiency causes a chronic subclinical proinflammatory age-associated state and, consequently, greater susceptibility to stressors. This work provides the molecular bases to further understand hearing disorders linked to IGF-1 deficiency.

scholarly journals Oxidative Stress Mediates Vascular Tortuosity

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 926
Author(s):  
Toshio Fumoto ◽  
Shouhei Kinoshita ◽  
Takao Sasaki ◽  
Norihito Shimamura ◽  
Hiroki Ohkuma
Keyword(s):  
Oxidative Stress ◽  
Basilar Artery ◽  
Morphological Changes ◽  
Imaging Techniques ◽  
Pcr Analysis ◽  
Adult Rats ◽  
Vascular Tortuosity ◽  
Bilateral Common Carotid Artery ◽  
Stress Related Genes ◽  
Underlying Mechanisms

Vascular tortuosity is associated with various disorders and is being increasingly detected through advances in imaging techniques. The underlying mechanisms for vascular tortuosity, however, remain unclear. Here, we tested the hypothesis that oxidative stress mediates the generation of tortuous vessels. We used the bilateral common carotid artery (CCA) ligation model to induce vascular tortuosity. Both young and adult rats showed basilar artery tortuous morphological changes one month after bilateral CCA ligation. These tortuous changes were permanent but more pronounced in the adult rats. Microarray and real-time PCR analysis revealed that these tortuous changes were accompanied by the induction of oxidative stress-related genes. Moreover, the indicated model in rabbits showed that tortuous morphological changes to the basilar artery were suppressed by antioxidant treatment. These results are highly suggestive of the significance of oxidative stress in the development of vascular tortuosity. Although further studies will be needed to elucidate the possible mechanisms by which oxidative stress enhances vascular tortuosity, our study also points toward possible prophylaxis and treatment for vascular tortuosity.

QT Prolongation in Dialysis Patients: An Epidemiological Study with a Focus on Malnutrition

2021 ◽  
pp. 1-8
Author(s):  
Masanori Shibata ◽  
Isao Ito ◽  
Hisae Tawada ◽  
Shinkichi Taniguchi
Keyword(s):  
Risk Index ◽  
Bioelectrical Impedance ◽  
Impedance Analysis ◽  
Serum Levels ◽  
Qt Prolongation ◽  
Fat Free Mass ◽  
Nutritional Risk ◽  
Diabetic Patients ◽  
Qtc Interval ◽  
Nutritional Risk Index

<b><i>Background/Aims:</i></b> QT prolongation is a known risk factor for ventricular fibrillation and ventricular tachycardia. Therefore, more refined management is necessary to reduce sudden cardiac death secondary to such arrhythmias. <b><i>Methods:</i></b> Electrocardiographic findings were reviewed in 224 patients, and the associations of QT prolongation with various clinical parameters were examined, including the nutritional state. Correlations were also examined between QT prolongation and body composition measurements determined by multifrequency bioelectrical impedance analysis. <b><i>Results:</i></b> Prolongation of the corrected QT (QTc) interval over 0.44 s was seen in 140 patients (62.5%). QT prolongation was independent of age and dialysis therapy duration and was more frequent in diabetics (70.1%) than in nondiabetics (54.2%, <i>p</i> = 0.014) and more frequent in women (78.8%) than in men (53.5%, <i>p</i> &#x3c; 0.001). Serum levels of albumin (<i>p</i> &#x3c; 0.001) and Cr (<i>p</i> &#x3c; 0.001) and the Geriatric Nutritional Risk Index (GNRI, <i>p</i> &#x3c; 0.001) were negatively correlated with QTc interval; no significant correlation was noted with total protein, urea nitrogen, or uric acid. Negative correlations with QTc interval were found for BMI(<i>p</i> &#x3c; 0.01), percent total body water (%TBW; <i>p</i> &#x3c; 0.05), and percent intracellular water (%ICW; <i>p</i> &#x3c; 0.01) but not with the percent extracellular water/TBW ratio or edema ratio. The longer the QTc interval, the lower the fat-free mass (FFM; <i>p</i> &#x3c; 0.01) and muscle mass (MM; <i>p</i> &#x3c; 0.01), but there was no significant correlation with percent fat. <b><i>Conclusion:</i></b> These results suggest that QT prolongation is a common complication and is more frequent in women and diabetic patients. The decreases in serum albumin and Cr levels, GNRI, BMI, %TBW, %ICW, FFM, and MM together coincided with malnutrition and thus suggest a close relationship of QT prolongation with malnutrition. Management of QT prolongation may be achieved better in the future by understanding these biochemical and biophysical changes, particularly those regarding malnutrition.

scholarly journals The Relationship between Frequently Used Glucose-Lowering Agents and Gut Microbiota in Type 2 Diabetes Mellitus

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
You Lv ◽  
Xue Zhao ◽  
Weiying Guo ◽  
Ying Gao ◽  
Shuo Yang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Short Chain Fatty Acids ◽  
Current Evidence ◽  
Diabetic Patients ◽  
Glucose Lowering ◽  
Patients With Diabetes ◽  
Gastrointestinal Side Effects ◽  
Underlying Mechanisms

Metabolic diseases, especially diabetes mellitus, have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or environmental factors. Current evidence suggests the association of gut microbiota with metabolic diseases. However, the effects of glucose-lowering agents on gut microbiota are poorly understood. Several studies revealed that these agents affect the composition and diversity of gut microbiota and consequently improve glucose metabolism and energy balance. Possible underlying mechanisms include affecting gene expression, lowering levels of inflammatory cytokines, and regulating the production of short-chain fatty acids. In addition, gut microbiota may alleviate adverse effects caused by glucose-lowering agents, and this can be especially beneficial in diabetic patients who experience severe gastrointestinal side effects and have to discontinue these agents. In conclusion, gut microbiota may provide a novel viewpoint for the treatment of patients with diabetes mellitus.

An investigation of the inflammatory cytokine and chemokine network in systemic sclerosis

2011 ◽  
Vol 70 (6) ◽  
pp. 1115-1121 ◽  
Author(s):  
Veronica Codullo ◽  
Helen M Baldwin ◽  
Mark D Singh ◽  
Alasdair R Fraser ◽  
Catherine Wilson ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Mononuclear Cells ◽  
Platelet Rich Plasma ◽  
Critical Role ◽  
Serum Levels ◽  
Pcr Analysis ◽  
Peripheral Blood Mononuclear ◽  
Matrix Deposition ◽  
Disease Subtype ◽  
Inflammatory Chemokines

ObjectivesSystemic sclerosis (SSc) is characterised by vasculopathy, an aberrantly activated immune system and excessive extracellular matrix deposition. Inflammatory chemokines control migration of cells to sites of tissue damage; their removal from inflamed sites is essential for resolution of the inflammatory response. The atypical chemokine receptor D6 has a critical role in this physiological balance. To explore potential deregulation of this system in SSc, inflammatory chemokine and D6 expression were compared with that in healthy controls (HC).MethodsSerum levels of inflammatory mediators were assessed by luminex analysis. Peripheral blood mononuclear cells (PBMCs) were used in molecular and immunocytochemical analysis. Platelet-rich plasma was collected and assessed by western blotting for D6 expression levels. Sex-matched HC were used for comparison.Results72 patients with SSc and 30 HC were enrolled in the study. The chemokines MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4 and IL-8/CXCL8 were significantly increased in patients with SSc, regardless of disease subtype and phase. Quantitative PCR analysis revealed a significant 10-fold upregulation of D6 transcripts in patients with SSc compared with controls, and this was paralleled by increased D6 protein expression in the PBMCs of patients with SSc. Platelet lysates also showed strong D6 expression in patients with SSc but not in controls. Importantly, high levels of D6 expression correlated with reduced levels of its ligands in serum.ConclusionsInflammatory chemokines and the regulatory receptor D6 are significantly upregulated in SSc and high D6 levels are associated with lower systemic chemokine levels, indicating that some patients control systemic chemokine levels using D6. These results suggest that chemokines may represent a therapeutic target in SSc.

Abstract P604: Astrocyte-dependent Regulation of Vascular Tone: Role in Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Juan Manuel Ramiro-Diaz ◽  
Ki Jung Kim ◽  
Jessica A Filosa
Keyword(s):  
Vascular Tone ◽  
Structural Changes ◽  
Neurovascular Unit ◽  
Brain Slices ◽  
Vascular Cognitive Impairment ◽  
Vascular Density ◽  
Aqp4 Expression ◽  
Functional Changes ◽  
Functional Studies ◽  
Underlying Mechanisms

Clinical studies support that untreated hypertension (HT) accelerates the development of vascular cognitive impairment (VCI). Yet, the underlying mechanisms for VCI are not known. In a recent study we demonstrated the role of astrocytes in the regulation of parenchymal arteriole (PA) steady-state vascular tone. Here we hypothesized hypertension results in structural and functional changes to the neurovascular unit resulting in enhanced astrocytic TRPV4 channel-dependent Ca 2+ increases contributing to augmented pressure-induced PA constriction . Functional studies were conducted in brain slices from angiotensin II (AngII) treated mice (600 ng/Kg/min, 28 days). PA arterioles within brain slices were perfused and pressurized and myogenic-evoked diameter changes measured using video microscopy. In addition, using the GLAST-CreERT2 ; R26-lsl-GCaMP3 mice we measure myogenic-evoked Ca 2+ changes in perivascular astrocytes. We demonstrate that HT increases pressure-induced PA tone by 11.14% at 30 mmHg and 12.97% at 60 mmHg (10.88 to 22.02 and 15.46 to 28.43% of tone, P<0.05 and P<0.01, respectively). In ANG II-treated mice, PA myogenic-evoked responses significantly increased astrocytic Ca 2+ oscillations frequency (119.4%, 0.0366 to 0.0803 Hz, P<0.0001). A significant increase in astrocytic Ca 2+ oscillation frequency was also observed after 2 min of AngII (500 nM) bath application (44.8%, 0.0366 to 0.053 Hz, P<0.01) in brain slices from AngII treated mice. Furthermore, using the model of spontaneous hypertensive rat (SHR) we observed that HT differentially increases vascular density and the number of vascular pericytes in cortical layers with highest neuronal densities (L III-V). Finally, while aquaporin 4 (AQP4) expression pattern was not different in the gray matter of SHR compared with WKY rats, a significant increase in unpolarized AQP4 expression was observed in the white matter of SHR. Taken together, this evidence indicates that HT induces functional and structural changes to the neurovascular unit favoring the development of regional brain hypoperfusion likely contributing to the development of VCI.

Abstract 1742: Expression of the Anti-Angiogenic Proteins Angiostatin and Endostatin is Increased in Diabetic Patients and Associated with Impaired Coronary Collateral Formation

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Neel R Sodha ◽  
Munir Boodhwani ◽  
Richard T Clements ◽  
Shu-Hua Xu ◽  
Roger L Laham ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Serum Levels ◽  
Diabetic Patients ◽  
Angiogenic Therapy ◽  
Collagen Xviii ◽  
Mmp9 Expression ◽  
Angiogenic Proteins ◽  
Incomplete Revascularization ◽  
Artery Disease

Introduction: Coronary artery disease is the leading cause of mortality in diabetics. Due to the diffuse nature of their disease, diabetics may be at risk for incomplete revascularization, highlighting a potential role for pro-angiogenic therapy in this group. This study investigates molecular mechanisms of angiogenesis in diabetics. Methods: Myocardial tissue was harvested from patients undergoing CABG (non-diabetic (ND) 11, type 2 diabetic (DM) 10). Expression of angiostatin, endostatin, their precursors (plasminogen and collagen XVIII, respectively), enzymes leading to their production (Matrix Metalloprotease (MMP) 2 & 9), and an inhibitor of MMPs (TIMP2) was assessed with western blotting. MMP activity was assessed. Serum levels of angiostatin and endostatin were assayed. Coronary collateralization was graded by Rentrop scoring of angiograms. Results: Plasminogen and collagen XVIII expression were similar between groups. Angiostatin expression trended to increase 1.24-fold (p=0.07) and endostatin expression increased 2.02-fold in DM patients relative to ND (p=0.02). Serum angiostatin was 2.68-fold higher (p=0.03) and endostatin 1.39-fold higher (p=0.04) in diabetics. MMP9 expression was no different between groups, whereas MMP2 expression decreased 1.8-fold in diabetics (p=0.003). MMP2 & 9 activity decreased 1.33-fold (p=0.03) and 1.57-fold (p=0.04), respectively, in diabetics. Coronary collateralization scores were ND 2.1 ± 0.37 vs. DM 1.0 ± 0.4 (p=0.05). Myocardial endostatin expression correlated strongly with %HbA1c (R=0.742, p=0.0001). Myocardial expression of angiostatin and endostatin demonstrated significant negative linear correlations with coronary collateralization (angiostatin R=−0.531, p=0.035, endostatin R=−0.794, p=0.0002). Conclusion: Diabetics exhibit increased levels of the anti-angiogenic proteins angiostatin and endostatin and differential regulation of the enzymes governing their production relative to non-diabetics. Myocardial levels of these proteins show significant correlation to coronary collateralization. These findings offer potential new therapeutic targets for enhancing pro-angiogenic therapy and insight in to the angiogenic impairments seen in diabetes.

MO580HYPOPROTEIC DIET SUPPLEMENTED WITH KETOANALOGUES IN PATIENTS WITH ADVANCED DIABETIC KIDNEY DISEASE – EFFECTS ON MINERAL BONE DISORDERS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Liliana Garneata ◽  
Carmen-Antonia Mocanu ◽  
Tudor Petrisor Simionescu ◽  
Andreea Elena Mocanu ◽  
Gabriel Mircescu
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Serum Levels ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Diabetic Patients ◽  
Bone Disorders ◽  
Diabetic Kidney ◽  
Low Protein ◽  
Ckd Stage

Abstract Background and Aims Dietary protein restriction is rediscussed as mainstay approach in advanced Chronic Kidney Disease (CKD), both in diabetics and non-diabetics to defer renal replacement therapy (RRT), mainly by better metabolic control; improvements in mineral bone disorders (MBD) were also suggested, but less studied in Diabetic Kidney Disease (DKD). An unicentric prospective interventional trial aimed to assess the effects of ketoanalogue-supplemented low protein diet (sLPD) on proteinuria and CKD progression (data already presented). The parameters of MBD were also evaluated. Method Adult diabetic patients (452) with stable CKD stage 4+, proteinuria&gt;3g/g creatininuria and SGA A were enrolled in a run-in phase (3 mo), with LPD (0.6g/kg dry ideal bw). Those who proved adherent (92, 64% males, median age 55.7 yrs, 65% on insulin) received sLPD (Ketosteril®, 1 tablet/10kg) for 12mo. Monitoring and treatment followed the Best Practice Guidelines. The primary endpoint was proteinuria during intervention as compared to pre-enrolment. Serum levels of calcium, phosphates and iPTH were considered to assess MBD. Nutrition, inflammation (SGA, BMI, serum albumin, CRP) and compliance were safety parameters. Results In patients with advanced DKD and severe proteinuria, sLPD was associated with a 69 (63; 82) % reduction in proteinuria (data presented). Significant amelioration in MBD was noted: serum levels of calcium and phosphates were significantly ameliorated at the end of the study as compared to enrolment - 4.3 (4.2-4.9) vs 3.2 (3.1-3.5) mg/dL and 5.4 (4.9-6.1) vs 8.2 (7.8-8.9) mg/dL, respectively. Serum iPTH significantly decreased: 185 (168-212) vs 375 (354-585) pg/mL. The need for calcium supplementation decreased: 6.5 (6.0-6.7) vs 7.0 (6.8-7.3) g/day. Vitamin D was required by only 35% vs 65% of patients. Nutritional status was preserved and dietary compliance was very good throughout the study. Conclusion In patients with advanced DKD ketoanalogue supplemented low protein diet seems to be effective and safe as part of MBD management.

Immunoreactive IGF-II in serum of healthy subjects and patients with growth hormone disturbances and uraemia

1984 ◽  
Vol 107 (2) ◽  
pp. 164-170 ◽  
Author(s):  
Gösta Enberg ◽  
Kerstin Hall
Keyword(s):  
Confidence Limit ◽  
Binding Protein ◽  
Protein S ◽  
Serum Levels ◽  
Cross Reaction ◽  
Diabetic Patients ◽  
Serum Samples ◽  
Igf I ◽  
Age Dependent ◽  
The Mean

Abstract. A radioimmunoassay has been developed for IGF-II, using Sepharose-coupled antibodies. Porcine insulin, human insulin and human proinsulin showed no cross-reaction, whereas the cross-reaction for IGF-I was 10%. To minimize the influence of the binding protein(s), all serum samples were extracted with acid ethanol before assay. The mean serum level of immunoreactive IGF-II and 95% confidence limit in 46 healthy adults were 587 ng/ml and 354–974 ng/ml, respectively. In contrast to the declining levels of IGF-I with increasing age, no such age-dependent decrease was found for IGF-II levels between 20 to 70 years. No difference in IGF-II levels was found between patients with acromegaly and healthy adult controls. In cord serum and serum from adult patients with GH deficiency the levels were significantly lower (P < 0.001) compared to controls. In diabetic patients with uraemia the mean level and 95% confidence limit were 1222 ng/ml and 532–2808 ng/ml, respectively. Thus, significantly increased serum levels of immunoreactive IGF-II have only been found in serum from patients with uraemia. Whether this is due to an increased production of IGF-II, or secondary to other factors such as the binding protein(s), will require further investigation.

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