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1.
Beside functional and structural changes in vascular biology,
alterations in the rheologic properties of blood cells
mainly determines to an impaired microvascular blood
flow in patients suffering from diabetes mellitus. Recent
investigations provide increasing evidence that impaired
C-peptide secretion in type 1 diabetic patients might contribute
to the development of microvascular complications.
C-peptide has been shown to stimulate endothelial
NO secretion by activation of the Ca2+ calmodolin regulated
enzyme eNOS. NO himself has the potency to increase
cGMP levels in smooth muscle cells and to activate
Na+ K+ ATPase activity and therefore evolves numerous effects
in microvascular regulation. In type 1 diabetic patients,
supplementation of C-peptide was shown to improve endothelium
dependent vasodilatation in an NO-dependent
pathway in different vascular compartments. In addition,
it could be shown that C-peptide administration in type 1
diabetic patients, results in a redistribution of skin blood
flow by increasing nutritive capillary blood flow in favour
to subpapillary blood flow. Impaired Na+ K+ ATPase in another
feature of diabetes mellitus in many cell types and
is believed to be a pivotal regulator of various cell functions.
C-peptide supplementation has been shown to restore
Na+ K+ATPase activity in different cell types during
in vitro and in vivo investigations. In type 1 diabetic patients,
C-peptide supplementation was shown to increase
erythrocyte Na+ K+ATPase activity by about 100%. There
was found a linear relationship between plasma C-peptide
levels and erythrocyte Na+ K+ATPase activity. In small
capillaries, microvascular blood flow is increasingly determined
by the rheologic properties of erythrocytes. Using laser-diffractoscopie a huge improvement in erythrocyte deformability
could be observed after C-peptide administration
in erythrocytes of type 1 diabetic patients. Inhibition
of the Na+ K+ATPase by Obain completely abolished the
effect of C-peptide on erythrocyte deformability. In conclusion,
C-peptide improves microvascular function and blood
flow in type 1 diabetic patients by interfering with vascular
and rheological components of microvascular blood flow. 相似文献
2.
P. Vague T. C. Coste M. F. Jannot D. Raccah M. Tsimaratos 《Experimental diabetes research》2004,5(1):37-50
Na+,K+-ATPase is an ubiquitous membrane enzyme
that allows the extrusion of three sodium ions from the cell
and two potassium ions from the extracellular fluid. Its activity
is decreased in many tissues of streptozotocin-induced
diabetic animals. This impairment could be at least partly
responsible for the development of diabetic complications.
Na+,K+-ATPase activity is decreased in the red blood cell
membranes of type 1 diabetic individuals, irrespective of the
degree of diabetic control. It is less impaired or even normal
in those of type 2 diabetic patients. The authors have
shown that in the red blood cells of type 2 diabetic patients,
Na+,K+-ATPase activity was strongly related to blood C-peptide
levels in non–insulin-treated patients (in whom C-peptide
concentration reflects that of insulin) as well as in
insulin-treated patients. Furthermore, a gene-environment
relationship has been observed. The alpha-1 isoform of the
enzyme predominant in red blood cells and nerve tissue is
encoded by the ATP1A1 gene.Apolymorphism in the intron
1 of this gene is associated with lower enzyme activity in patients
with C-peptide deficiency either with type 1 or type
2 diabetes, but not in normal individuals. There are several
lines of evidence for a low C-peptide level being responsible
for low Na+,K+-ATPase activity in the red blood cells.
Short-term C-peptide infusion to type 1 diabetic patients
restores normal Na+,K+-ATPase activity. Islet transplantation,
which restores endogenous C-peptide secretion, enhances
Na+,K+-ATPase activity proportionally to the rise
in C-peptide. This C-peptide effect is not indirect. In fact,
incubation of diabetic red blood cells with C-peptide at
physiological concentration leads to an increase of Na+,K+-ATPase activity. In isolated proximal tubules of rats or
in the medullary thick ascending limb of the kidney, C-peptide stimulates in a dose-dependent manner Na+,K+-ATPase activity. This impairment in Na+,K+-ATPase activity,
mainly secondary to the lack of C-peptide, plays probably
a role in the development of diabetic complications.
Arguments have been developed showing that the diabetesinduced
decrease in Na+,K+-ATPase activity compromises
microvascular blood flow by two mechanisms: by affecting
microvascular regulation and by decreasing red blood cell
deformability, which leads to an increase in blood viscosity.
C-peptide infusion restores red blood cell deformability
and microvascular blood flow concomitantly with Na+,K+-ATPase activity. The defect in ATPase is strongly related to
diabetic neuropathy. Patients with neuropathy have lower
ATPase activity than those without. The diabetes-induced
impairment in Na+,K+-ATPase activity is identical in red
blood cells and neural tissue. Red blood cell ATPase activity
is related to nerve conduction velocity in the peroneal
and the tibial nerve of diabetic patients. C-peptide infusion
to diabetic rats increases endoneural ATPase activity in rat.
Because the defect in Na+,K+-ATPase activity is also probably
involved in the development of diabetic nephropathy and
cardiomyopathy, physiological C-peptide infusion could be
beneficial for the prevention of diabetic complications. 相似文献
3.
Photobiomodulation induces antinociception,recovers structural aspects and regulates mitochondrial homeostasis in peripheral nerve of diabetic mice
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Victória R. da Silva Oliveira Diego P. Cury Laura B. Yamashita Marcos V. Esteca Ii‐Sei Watanabe Yoko Fee Bergmann Elaine F. Toniolo Camila S. Dale 《Journal of biophotonics》2018,11(9)
Diabetic peripheral neuropathy (DPN) is a nervous disorder caused by diabetes mellitus, affecting about 50% of patients in clinical medicine. Chronic pain is one of the major and most unpleasant symptoms developed by those patients, and conventional available treatments for the neuropathy, including the associated pain, are still unsatisfactory and benefit only a small number of patients. Photobiomodulation (PBM) has been gaining clinical acceptance once it is able to promote early nerve regeneration resulting in significant improvement in peripheral nerves disabilities. In this work, the effects of PBM (660 nm, 30 mW, 1.6 J/cm2, 0.28 cm2, 15 s in a continuous frequency) on treating DPN‐induced pain and nerve damage were evaluated in an experimental model of diabetic‐neuropathy induced by streptozotocin in mice. PBM‐induced antinociception in neuropathic‐pain mice was dependent on central opioids release. After 21 consecutive applications, PBM increased nerve growth factor levels and induced structural recovery increasing mitochondrial content and regulating Parkin in the sciatic nerve of DPN‐mice. Taking together, these data provide new insights into the mechanisms involved in the effects of PBM‐therapy emphasizing its therapeutic potential in the treatment of DPN. 相似文献
4.
The prevalence of diabetes has reached epidemic proportions. There are two forms of diabetes: type 1 diabetes mellitus is due to auto-immune-mediated destruction of pancreatic β-cells resulting in absolute insulin deficiency and type 2 diabetes mellitus is due to reduced insulin secretion and or insulin resistance. Both forms of diabetes are characterized by chronic hyperglycemia, leading to the development of diabetic peripheral neuropathy (DPN) and microvascular pathology. DPN is characterized by enhanced or reduced thermal, chemical, and mechanical pain sensitivities. In the long-term, DPN results in peripheral nerve damage and accounts for a substantial number of non-traumatic lower-limb amputations. This review will address the mechanisms, especially the role of reactive oxygen and nitrogen species in the development and progression of DPN. 相似文献
5.
W. Zhang M. Yorek C. R. Pierson Y. Murakawa A. Breidenbach A. A. F. Sima 《Experimental diabetes research》2001,2(3):187-193
In order to explore the neuroprotective and crossspecies
activities of.C-peptide on type 1 diabetic
neuropathy, spontaneously diabetic BB/W-rats were
given increasing doses of human recombinant Cpeptide
(hrC-peptide). Diabetic rats received 10, 100,
500, or 1000 μg of hrC-peptide/kg body weight/
day from onset of diabetes. After 2 months of hrC-peptide
administration, 100 μg and greater doses
completely prevented the nerve conduction defect,
which was associated with a significant but incomplete
prevention of neural Na+/K+-ATPase activity
in diabetic rats with 500 μg or greater C-peptide replacement.
Increasing doses of hrC-peptide showed
increasing prevention of early structural abnormalities
such as paranodal swelling and axonal degeneration
and an increasing frequency of regenerating
sural nerve fibers. We conclude that hrC-peptide exerts
a dose dependent protection on type 1 diabetic
neuropathy in rats and that this effect is probably
mediated by the partially conserved sequence of the
active C-terminal pentapeptide 相似文献
6.
Substantial evidence collected from clinical data and experimental
studies has indicated that CNS is not spared
from diabetes complications. Impairments in CNS function
are well documented in both type 1 and type 2 diabetic
patients as well as in various animal models of diabetes,
in terms of alterations in cognition, neuropsychology, neurobehavior,
electrophysiology, structure, neurochemistry
and apoptotic activities. These data suggest that primary
diabetic encephalopathy exists as a definable diabetic complication.
The mechanisms underlying this CNS complication
are not clear. Experimental studies have suggested that
neuronal apoptosis may play an important role in neuronal
loss and impaired cognitive function. In diabetes multiple
factors are responsible for neuronal apoptosis, such as a perturbed
IGF system, hyperglycemia and the aging process
itself. Recent data suggest that insulin/C-peptide deficiency
may exert an eminent role. Administration of C-peptide
partially corrects the perturbed IGF system in the brain
and prevents neuronal apoptosis in hippocampus of type 1
diabetes. In neuroblastoma SH-SY5Y cells C-peptide provides
a dose-dependent stimulation on cell proliferation and
an anti-apoptotic effect as well. These studies provide a basis
for administration of C-peptide as a potentially effective
therapy for type 1 diabetes. 相似文献
7.
8.
《The Journal of nutritional biochemistry》2014,25(7):765-772
Diabetic peripheral neuropathy (DPN) is the most common and troublesome complication of type 2 diabetes mellitus (T2DM). Recent findings reveal an important role of endoplasmic reticulum (ER) stress in the development of DPN and identify a potential new therapeutic target. Schwann cells (SC), the myelinating cells in peripheral nervous system, are highly susceptible to ER homeostasis. Grape seed proanthocyanidins (GSPs) have been reported to improve DPN of type 1 diabetic rats and relieve ER stress in skeletal muscles and pancreas of T2DM. We investigated the potential role of ER stress in SC in regulating DPN of T2DM and assessed whether early intervention of GSPs would prevent DPN by modulating ER stress. The present study was performed in Sprague–Dawley rats made T2DM with low-dose streptozotocin and a high-carbohydrate/high-fat diet and in rat SC cultured in serum from type 2 diabetic rats. Diabetic rats showed a typical characteristic of T2DM and slowing of nerve conduction velocity (NCV) in sciatic/tibial nerves. The lesions of SC, Ca2+ overload and ER stress were present in sciatic nerves of diabetic rats, as well as in cell culture models. GSPs administration significantly decreased the low-density lipoprotein level and increased NCV in diabetic rats. GSPs or their metabolites also partially prevented cell injury, Ca2+ overload and ER stress in animal and cell culture models. Therefore, ER stress is implicated in peripheral neuropathy in animal and cell culture models of T2DM. Prophylactic GSPs treatment might have auxiliary preventive potential for DPN partially by alleviating ER stress. 相似文献
9.
Stevens MJ Zhang W Li F Sima AA 《American journal of physiology. Endocrinology and metabolism》2004,287(3):E497-E505
Oxidative stress and neurovascular dysfunction have emerged as contributing factors to the development of experimental diabetic neuropathy (EDN) in streptozotocin-diabetic rodents. Additionally, depletion of C-peptide has been implicated in the pathogenesis of EDN, but the mechanisms of these effects have not been fully characterized. The aims of this study were therefore to explore the effects of diabetes on neurovascular dysfunction and indexes of nerve oxidative stress in type 1 bio-breeding Worcester (BB/Wor) rats and type 2 BB Zucker-derived (ZDR)/Wor rats and to determine the effects of C-peptide replacement in the former. Motor and sensory nerve conduction velocities (NCVs), hindlimb thermal thresholds, endoneurial blood flow, and indicators of oxidative stress were evaluated in nondiabetic control rats, BB/Wor rats, BB/Wor rats with rat II C-peptide replacement (75 nmol C-peptide.kg body wt(-1).day(-1)) for 2 mo, and diabetes duration-matched BBZDR/Wor rats. Endoneurial perfusion was decreased and oxidative stress increased in type 1 BB/Wor rats. C-peptide prevented NCV and neurovascular deficits and attenuated thermal hyperalgesia. Inhibition of nitric oxide (NO) synthase, but not cyclooxygenase, reversed the C-peptide-mediated effects on NCV and nerve blood flow. Indexes of oxidative stress were unaffected by C-peptide. In type 2 BBZDR/Wor rats, neurovascular deficits and increased oxidative stress were unaccompanied by sensory NCV slowing or hyperalgesia. Therefore, nerve oxidative stress is increased and endoneurial perfusion decreased in type 1 BB/Wor and type 2 BBZDR/Wor rats. NO and neurovascular mechanisms, but not oxidative stress, appear to contribute to the effects of C-peptide in type 1 EDN. Sensory nerve deficits are not an inevitable consequence of increased oxidative stress and decreased nerve perfusion in a type 2 diabetic rodent model. 相似文献
10.
Tao Lei Da Jing Kangning Xie Maogang Jiang Feijiang Li Jing Cai Xiaoming Wu Chi Tang Qiaoling Xu Juan Liu Wei Guo Guanghao Shen Erping Luo 《PloS one》2013,8(4)
Although numerous clinical studies have reported that pulsed electromagnetic fields (PEMF) have a neuroprotective role in patients with diabetic peripheral neuropathy (DPN), the application of PEMF for clinic is still controversial. The present study was designed to investigate whether PEMF has therapeutic potential in relieving peripheral neuropathic symptoms in streptozotocin (STZ)-induced diabetic rats. Adult male Sprague–Dawley rats were randomly divided into three weight-matched groups (eight in each group): the non-diabetic control group (Control), diabetes mellitus with 15 Hz PEMF exposure group (DM+PEMF) which were subjected to daily 8-h PEMF exposure for 7 weeks and diabetes mellitus with sham PEMF exposure group (DM). Signs and symptoms of DPN in STZ-treated rats were investigated by using behavioral assays. Meanwhile, ultrastructural examination and immunohistochemical study for vascular endothelial growth factor (VEGF) of sciatic nerve were also performed. During a 7-week experimental observation, we found that PEMF stimulation did not alter hyperglycemia and weight loss in STZ-treated rats with DPN. However, PEMF stimulation attenuated the development of the abnormalities observed in STZ-treated rats with DPN, which were demonstrated by increased hind paw withdrawal threshold to mechanical and thermal stimuli, slighter demyelination and axon enlargement and less VEGF immunostaining of sciatic nerve compared to those of the DM group. The current study demonstrates that treatment with PEMF might prevent the development of abnormalities observed in animal models for DPN. It is suggested that PEMF might have direct corrective effects on injured nerves and would be a potentially promising non-invasive therapeutic tool for the treatment of DPN. 相似文献
11.
12.
目的:观察光子中医信息疗法对糖尿病周围神经病变患者的临床疗效。方法:将60例符合入选标准的患者,以1∶1的比例随机分配到治疗组(光子中医信息疗法联合药物组)、对照组(药物组),两组患者均给予糖尿病基础治疗,对照组加甲钴胺口服,每次500μg,每日3次,疗程4周;治疗组在对照组的基础上配合光子中医信息疗法,隔日照射1次,每周3次,6次为1疗程,共2个疗程。治疗前后分别对两组患者的中医临床症状、神经症状体征进行评定,并测定周围神经传导速度及观察血糖变化情况,进行综合疗效评估。结果:治疗组的临床综合疗效明显优于对照组,两组的总有效率比较有显著性差异(P<0.05)。治疗组在中医症状改善、周围神经症状及体征改善、提高周围神经传导速度方面均优于对照组,组间比较均具有显著性差异(P<0.05)。治疗后治疗组空腹血糖、餐后血糖、糖化血红蛋白与治疗前比较均明显降低(P<0.01),对照组治疗前后比较及治疗后组间比较均无显著性差异(P>0.05)。结论:光子中医信息疗法联合药物组相对于药物组在改善DPN患者的临床症状、周围神经症状及体征、神经的传导速度等方面均有良好的优势,同时具有一定的辅助降糖趋势。 相似文献
13.
Kimura K Niijima A Yoshida R Kitamura T Kamikawa A Furuya DT Kitamura N Konno A Nakamoto H Sakane N Yoshida T Saito M 《Peptides》2005,26(12):2547-2553
The aim of this study was to examine the effect of proinsulin C-peptide on the autonomic nervous systems in rats. Intravenous administration of C-peptide gradually increased electrophysiological activity of the vagus nerves into the stomach and pancreas for at least 90 min. It also slightly increased gastric acid secretion that was suppressed by the treatment with atropine. Intraperitoneal injection of C-peptide did not affect the basal and stress-induced norepinephrine (NE) turnover rate, a biochemical index of sympathetic nerve activity. These results indicate that C-peptide increases parasympathetic nerve activity without affecting sympathetic nerve activity. This could explain, at least in part, the ameliorating effects of C-peptide on impaired cardiac autonomic nerve functions in patients with type 1 diabetes. 相似文献
14.
Tarek Kamal Motawi Sherine Maher Rizk Ihab Abdel‐Rahman Ibrahim Yasmin Farid El‐Emady 《Cell biochemistry and function》2014,32(2):155-163
Diabetic peripheral neuropathy (DPN) is one of the most common diabetic chronic complications. There is an increased attention directed towards the role of angiogenic factors including vascular endothelial growth factor (VEGF) and anti‐angiogenic factors including soluble endoglin (sEng) as contributors to diabetic microvascular complications including neuropathy. The purposes of this study were to determine the role of these angiogenesis regulators in the prognosis of DPN. The study group included 60 patients with type 2 diabetes mellitus (T2DM) and 20 clinically healthy individuals. The patients were divided into two groups. Group I included 20 T2DM patients without peripheral neuropathy, and Group II consisted of 40 T2DM patients with DPN. In all groups, plasma VEGF, sEng and endothelin‐1 (ET‐1), nitric oxide and ET‐1 mRNA were estimated. Plasma levels of VEGF, sEng, ET‐1 and nitric oxide were significantly elevated in diabetic patients (Groups I and II) compared with healthy control subjects, with a higher increase in their levels in patients with DPN compared with diabetic patients without peripheral neuropathy. Measurement of plasma levels of angiogenesis‐related biomarkers in high‐risk diabetic patients might identify who later develop DPN, thus providing opportunities for early detection and targets for novel treatments. Copyright © 2013 John Wiley & Sons, Ltd. 相似文献
15.
Lei Wang Michael Chopp Alexandra Szalad LongFei Jia XueRong Lu Mei Lu Li Zhang Yi Zhang RuiLan Zhang Zheng Gang Zhang 《PloS one》2015,10(2)
Diabetic peripheral neuropathy is a common complication of long-standing diabetes mellitus. To mimic clinical trials in which patients with diabetes enrolled have advanced peripheral neuropathy, we investigated the effect of sildenafil, a specific inhibitor of phosphodiesterase type 5 enzyme, on long term peripheral neuropathy in middle aged male mice with type II diabetes. Treatment of diabetic mice (BKS.Cg-m+/+Leprdb/J, db/db) at age 36 weeks with sildenafil significantly increased functional blood vessels and regional blood flow in the sciatic nerve, concurrently with augmentation of intra-epidermal nerve fiber density in the skin and myelinated axons in the sciatic nerve. Functional analysis showed that the sildenafil treatment considerably improved motor and sensory conduction velocities in the sciatic nerve and peripheral thermal stimulus sensitivity compared with the saline treatment. In vitro studies showed that mouse dermal endothelial cells (MDE) cultured under high glucose levels exhibited significant down regulation of angiopoietin 1 (Ang1) expression and reduction of capillary-like tube formation, which were completely reversed by sildenafil. In addition, incubation of dorsal root ganglia (DRG) neurons with conditioned medium harvested from MDE under high glucose levels suppressed neurite outgrowth, where as conditional medium harvested from MDE treated with sildenafil under high glucose levels did not inhibit neurite outgrowth of DRG neurons. Moreover, blockage of the Ang1 receptor, Tie2, with a neutralized antibody against Tie2 abolished the beneficial effect of sildenafil on tube formation and neurite outgrowth. Collectively, our data indicate that sildenafil has a therapeutic effect on long term peripheral neuropathy of middle aged diabetic mice and that improvement of neurovascular dysfunction by sildenafil likely contributes to the amelioration of nerve function. The Ang1/Tie2 signaling pathway may play an important role in these restorative processes. 相似文献
16.
Anders A. F. Sima George Grunberger Hans J?rnvall John Wahren The C-Peptide Study Group 《Experimental diabetes research》2001,2(2):145-151
In recent years the physiological role of the proinsulin
C-peptide has received increasing attention,
focusing on the potential therapeutic value of
C-peptide replacement in preventing and ameliorating
type 1 diabetic complications. In order to consolidate
these new data and to identify the immediate
directions of C-peptide research and its clinical
usefulness, an International Symposium was held
in Detroit, Michigan, on October 20–21, 2000, under
the auspices of the Wayne State University/Morris
Hood Jr. Comprehensive Diabetes Center. In this
communication, we review the cellular, physiological
and clinical effects of C-peptide replacement in
animal models and in patients with type 1 diabetes.
Finally, recommendations are presented as to the
most urgent studies that should be pursued to further
establish the biological action of C-peptide and
its therapeutic value. 相似文献
17.
Diabetic peripheral neuropathy (DPN) is one of the most common diabetic chronic complications. The pathogenesis of DPN is complex and involves an intertwined array of mechanisms. The purposes of this study were to evaluate the association of oxidative stress and vascular risk factors with the prevalence of DPN and to determine the role of these biochemical parameters in the prognosis of DPN. One hundred patients with type 2 diabetes mellitus and 40 clinically healthy individuals were evaluated. The patients were divided into two groups. Group 1 included 40 diabetic patients without peripheral neuropathy, and group 2 consisted of 60 patients with DPN. Erythrocytes glutathione (GSH) level, plasma malondialdehyde (MDA), nitrite/nitrate (NOx) and homocysteine (Hcy) levels as well as serum ceruloplasmin (Cp), total antioxidants (TAO), endothelin-1 (ET-1) levels and γ-glutamyl transferase (GGT) activity were estimated. A significant decrease of erythrocyte GSH was observed in groups 1 and 2 relative to the controls. An increase in glycosylated haemoglobin (HbA1c), MDA, NOx, GGT, Cp, TAO, Hcy and ET-1 was noted in patients with DPN. In conclusion, oxidative stress biomarkers and vascular risk factors could be important in the pathogenesis of DPN. The measurement of serum GGT and Hcy in addition to HbA1c and disease duration could facilitate the early detection of neuropathy in diabetic patients. 相似文献
18.
Ze-Peng Mu Yan-Gang Wang Cheng-Qian Li Wen-Shan Lv Bin Wang Zhao-Hai Jing Xue-Jia Song Yu Lun Ming-Yue Qiu Xiao-Long Ma 《Molecular neurobiology》2017,54(2):983-996
Tumor necrosis factor-α (TNF-α) is a cell signaling protein involved in systemic inflammation, and is also an important cytokine in the acute phase reaction. Several studies suggested a possible association between TNF-α and diabetic peripheral neuropathy (DPN) in type 2 diabetic patients, but no accurate conclusion was available. A systematic review and meta-analysis of observational studies was performed to comprehensively assess the association between serum TNF-α levels and DPN in type 2 diabetic patients. We searched Pubmed, Web of Science, Embase, and China Biology Medicine (CMB) databases for eligible studies. Study-specific data were combined using meta-analysis. Fourteen studies were finally included into the meta-analysis, which involved a total of 2650 participants. Meta-analysis showed that there were obviously increased serum TNF-α levels in DPN patients compared with type 2 diabetic patients without DPN (standard mean difference [SMD]?=?1.203, 95 % CI 0.795–1.611, P?<?0.001). There were also obviously increased levels of serum TNF-α in diabetic patients with DPN when compared with healthy controls (SMD?=?2.364, 95 % CI 1.333–3.394, P?<?0.001). In addition, there were increased serum TNF-α levels in painful DPN patients compared with painless DPN patients (SMD?=?0.964, 95 % CI 0.237–1.690, P?=?0.009). High level of serum TNF-α was significantly associated with increased risk of DPN in patients with type 2 diabetes (odds ratio [OR]?=?2.594, 95 % CI 1.182–5.500, P?=?0.017). Increased serum levels of TNF-α was not associated with increased risk of painful DPN in patients with type 2 diabetes (OR?=?2.486, 95 % CI 0.672–9.193, P?=?0.172). Sensitivity analysis showed that there was no obvious change in the pooled estimates when omitting single study by turns. Type 2 diabetic patients with peripheral neuropathy have obviously increased serum TNF-α levels than type 2 diabetic patients without peripheral neuropathy and healthy controls, and high level of serum TNF-α may be associated with increased risk of peripheral neuropathy independently. Further prospective cohort studies are needed to assess the association between TNF-α and DPN. 相似文献
19.
Spitsina EV Iakunina NIu Chudakova DA Nikitin AG Svetlova GN Soluianova TN Strokov IA Nosikov VV 《Molekuliarnaia biologiia》2007,41(6):989-993
The aim of this study was the search of association of polymorphous markers Pro72Arg and C(-594)CC of TP53 gene with diabetic polyneuropathy (DPN) in patients with type 1 diabetes mellitus with or without clinical signs of DPN. We have found that polymorphous marker Pro72Arg of TP53 gene was associated with DPN in Russian patients with type 1 diabetes mellitus living in Moscow. The carriers of Arg allele and Arg/Arg genotype had higher risk of DPN development (OR = 1.96; CI = 1.32-2.90; and OR = 2.14; CI = 1.23-3.73; relatively). On the contrary, the carriage of Pro allele was associated with the lower risk of DPN development (OR = 0.51; CI = 0.34-0.76). We have not found any association of polymorphous marker C(-594)CC of TP53 gene with DPN in Russian patients with type 1 diabetes mellitus living in Moscow. 相似文献
20.
John Wahren Jawed Shafqat Jan Johansson Alexander Chibalin Karin Ekberg Hans J?rnvall 《Experimental diabetes research》2004,5(1):15-23
New results present C-peptide as a biologically active
peptide hormone in its own right. Although C-peptide is
formed from proinsulin and cosecreted with insulin, it is a
separate entity with biochemical and physiological characteristics
that differ from those of insulin. There is direct
evidence of stereospecific binding of C-peptide to a
cell surface receptor, which is different from those for insulin
and other related hormones. The C-peptide binding
site is most likely a G–protein–coupled receptor. The association
constant for C-peptide binding is approximately
3 × 109M-1. Saturation of the binding occurs already at a
concentration of about 1 nM, which explains why C-peptide
effects are not observed in healthy subjects. Binding of C-peptide
results in activation of Ca2+ and MAPK-dependent
pathways and stimulation of Na+,K+-ATPase and eNOS
activities. The latter 2 enzymes are both deficient in several
tissues in type 1 diabetes. There is some evidence that
C-peptide, and insulin may interact synergistically on the
insulin signaling pathway. Clinical evidence suggests that
replacement of C-peptide, together with regular insulin
therapy, may be beneficial in patients with type 1 diabetes
and serve to retard or prevent the development of long-term
complications. 相似文献