Transient increase in renal insulin-like growth factor binding proteins during initial kidney hypertrophy in experimental diabetes in rats

Flyvbjerg, Allan; Kessler, Ulrike; Dorka, B; Funk, B.; Ørskov, Hans; Kieß, Wieland

doi:10.1007/bf00400489

Cited by 105 publications

(61 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This can be either local, due to increased translation of IGF-I mRNA, or circulating, due to an increased sequestration of IGF-I by IGF receptors or binding proteins (IGFBPs). IGF receptors mRNA [156] and IG-FBP expression [157] were found to be increased in short-term diabetes, though these data were not confirmed by other studies [155,158]. At variance with the early stages of the disease, very few studies have investigated the renal IGF system in advanced diabetes.…”

Section: Target Organ Manifestationsmentioning

confidence: 76%

15 th Golgi lecture: from hyperglycaemia to the dysregulation of vascular remodelling in diabetes

Mario

Pugliese

2001

Diabetologia

View full text Add to dashboard Cite

Hyperglycaemia has been shown to play a central part in diabetic vascular disease, which is also influenced by individual background. Hyperglycaemia initiates the pathogenetic sequence through a series of interrelated biochemical abnormalities, including increased flux through the polyol and hexosamine pathways, oxidative stress, AGE formation and protein kinase C activation. These abnormalities are capable of modifying the function of resident and non-resident vascular cells by changing their production pattern of several autocrine and paracrine factors, including growth, vasoactive and coagulation factors and adhesion molecules. These mediators profoundly impair the physiologic turnover of the vessel wall, thus leading to an abnormal process of vascular remodelling, with alterations in cell and matrix turnover and contacts, vascular tone and permeability and coagulation pattern. This process has distinct features depending on the target tissue. The hallmark of nephropathy is an abnormal accumulation of extracellular matrix within the mesangium, sustained by an upregulation of TGF-b, possibly triggered by a local activation of the renin-angiotensin system. The central pathological lesion in retinopathy is retinal ischaemia due to the formation of acellular capillaries. The resulting vascular endothelial growth factor-dependent neovascularization is a detrimental phenomenon leading to the formation of noncompetent vessels. Conversely, in macrovascular disease, arterial occlusion resulting from plaque formation with superimposed thrombosis elicits an angiogenic response which is impaired, but generates competent vessels, potentially compensating for reduced flow. Thus, upstream interventions interrupting the pathogenetic sequence at the level of hyperglycaemia (and related biochemical events) are the most effective, whereas downstream interventions should be targeted to the tissue affected. [Diabetologia (2001) 44: 674±692]

show abstract

Section: Target Organ Manifestationsmentioning

confidence: 76%

15 th Golgi lecture: from hyperglycaemia to the dysregulation of vascular remodelling in diabetes

Mario

Pugliese

2001

Diabetologia

View full text Add to dashboard Cite

show abstract

“…s-IGFBP-3 was measured by commercially available immunoradiometric assay (BioSource Europe, Nivelles, Belgium) (CV% within and between assay: Ͻ5 and Ͻ10%, respectively). Tendon dialysates were analyzed for IGFBP-1 to -4 by Western ligand blotting, as previously described (16). Serum was analyzed for PINP for indirect quantification of collagen synthesis in bone (s-PINP).…”

Section: Experimental Protocol and Methodsmentioning

confidence: 99%

Effect of estrogen on tendon collagen synthesis, tendon structural characteristics, and biomechanical properties in postmenopausal women

Hansen

Kongsgaard²,

Holm³

et al. 2009

Journal of Applied Physiology

121

114

View full text Add to dashboard Cite

Flyvbjerg A, Langberg H, Kjaer M. Effect of estrogen on tendon collagen synthesis, tendon structural characteristics, and biomechanical properties in postmenopausal women. J Appl Physiol 106: 1385-1393, 2009. First published October 16, 2009 doi:10.1152/japplphysiol.90935.2008.-The knowledge about the effect of estradiol on tendon connective tissue is limited. Therefore, we studied the influence of estradiol on tendon synthesis, structure, and biomechanical properties in postmenopausal women. Nonusers (control, n ϭ 10) or habitual users of oral estradiol replacement therapy (ERT, n ϭ 10) were studied at rest and in response to one-legged resistance exercise. Synthesis of tendon collagen was determined by stable isotope incorporation [fractional synthesis rate (FSR)] and microdialysis technique (NH2-terminal propeptide of type I collagen synthesis). Tendon area and fibril characteristics were determined by MRI and transmission electron microscopy, whereas tendon biomechanical properties were measured during isometric maximal voluntary contraction by ultrasound recording. Tendon FSR was markedly higher in ERT users (P Ͻ 0.001), whereas no group difference was seen in tendon NH2-terminal propeptide of type I collagen synthesis (P ϭ 0.32). In ERT users, positive correlations between serum estradiol (sestradiol) and tendon synthesis were observed, whereas change in tendon synthesis from rest to exercise was negatively correlated to s-estradiol. Tendon area, fibril density, fibril volume fraction, and fibril mean area did not differ between groups. However, the percentage of medium-sized fibrils was higher in ERT users (P Ͻ 0.05), whereas the percentage of large fibrils tended to be greater in control (P ϭ 0.10). A lower Young's modulus (GPa/%) was found in ERT users (P Ͻ 0.05). In conclusion, estradiol administration was associated with higher tendon FSR and a higher relative number of smaller fibrils. Whereas this indicates stimulated collagen turnover in the resting state, collagen responses to exercise were negatively associated with s-estradiol. These results indicate a pivotal role for estradiol in maintaining homeostasis of female connective tissue. connective tissue; tendon fibrils; insulin-like growth factor-I; extracellular matrix; bone CROSS-SECTIONAL FINDINGS INDICATE that sex hormones influence tendon biomechanical properties (36), extracellular matrix adaptability in response to mechanical loading (11,21,36,41,59), and the risk of sustaining soft tissue injuries (11,24,25).Estrogen receptors have been localized in ligaments (32, 33), and tendons express transcripts for estrogen receptors (23). Nevertheless, the effect of estrogen on tendon and ligament turnover is not clarified. Thus an inhibiting effect (34, 60), no effect (51), and a stimulating effect (32) on collagen synthesis and fibroblast proliferation in vitro have been observed in anterior cruciate ligament (ACL) tissue samples. These contrasting findings are probably related to the variation between animal species and the applied methods. This ...

show abstract

“…SDS-PAGE and Western ligand blotting (WLB) were performed as previously described (7,13). Two microliters of serum was subjected to SDS-PAGE (10% polyacrylamide) under nonreducing conditions.…”

Section: Methodsmentioning

confidence: 99%

Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats

Buhl¹,

Neschen²,

Yonemitsu³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Individuals born with a low birth weight (LBW) have an increased prevalence of type 2 diabetes, but the mechanisms responsible for this association are unknown. Given the important role of insulin resistance in the pathogenesis of type 2 diabetes, we examined insulin sensitivity in a rat model of LBW due to intrauterine fetal stress. During the last 7 days of gestation, rat dams were treated with dexamethasone and insulin sensitivity was assessed in the LBW offspring by a hyperinsulinemic euglycemic clamp. The LBW group had liver-specific insulin resistance associated with increased levels of PEPCK expression. These changes were associated with pituitary hyperplasia of the ACTHsecreting cells, increased morning plasma ACTH concentrations, elevated corticosterone secretion during restraint stress, and an ϳ70% increase in 24-h urine corticosterone excretion. These data support the hypothesis that prenatal stress can result in chronic hyperactivity of the hypothalamic-pituitary-adrenal axis, resulting in increased plasma corticosterone concentrations, upregulation of hepatic gluconeogenesis, and hepatic insulin resistance. gluconeogenesis; adrenocorticotropic hormone; corticosterone; type 2 diabetes ACCORDING TO THE BARKER HYPOTHESIS, harmful events taking place during the fetal period can induce life-long changes in different organs predisposing to development of disease (1). In accordance with this hypothesis, individuals born with a birth weight of less than 5.5 lbs [low birth weight (LBW)] are insulin resistant (3,12,15,17,22,28,30,35) and have increased prevalence of type 2 diabetes (10, 15, 28). Additionally, these patients are also prone to exhibit impaired growth in childhood and early adulthood, which may be related to alterations in the growth hormone/IGF-I homeostasis (16,18,20). The mechanisms responsible for these changes associated with LBW are unknown.Recently, fetal stress and high plasma levels of glucocorticoids have been suggested (5, 27) to lead to hypothalamicpituitary-adrenal (HPA) axis hyperactivity, which after birth may result in chronically excessive adrenal glucocorticoid secretion, and an increased risk for the development of type 2 diabetes. However, these findings have been contrasted by other studies that have found no change (32) or decreased HPA axis activity (21) in LBW rat models.To examine the mechanism and potential role of the HPA axis in causing LBW-associated insulin resistance, we assessed insulin-stimulated liver and muscle glucose metabolism, total IGF-I, and IGF-binding proteins (IGFBPs), as well as HPA axis activity in a rat model of stress-induced LBW. MATERIALS AND METHODS Animals.From day 7 of gestation, pregnant female Sprague-Dawley rats (Charles River, Wilmington, MA) were housed singly under temperature (22-23°C)-and light-controlled (12:12-h light-dark cycle) conditions. On day 14 of gestation, rats were randomized into three groups: control, dexamethasone treatment, or foster mother group. From day 14 to day 21 of gestation, a daily subcutaneously injection of d...

show abstract

Transient increase in renal insulin-like growth factor binding proteins during initial kidney hypertrophy in experimental diabetes in rats

Cited by 105 publications

References 9 publications

15 th Golgi lecture: from hyperglycaemia to the dysregulation of vascular remodelling in diabetes

15 th Golgi lecture: from hyperglycaemia to the dysregulation of vascular remodelling in diabetes

Effect of estrogen on tendon collagen synthesis, tendon structural characteristics, and biomechanical properties in postmenopausal women

Increased hypothalamic-pituitary-adrenal axis activity and hepatic insulin resistance in low-birth-weight rats

Contact Info

Product

Resources

About