Expression of adropin in rat brain, cerebellum, kidneys, heart, liver, and pancreas in streptozotocin-induced diabetes

Aydın, Süleyman; Kuloğlu, Tuncay; Eren, Mehmet Nesimi; Yılmaz, Musa; Kalaycı, Mehmet; Şahin, İ̇brahim; Kocaman, Nevin; Citil, Cihan; Kendir, Yalçın

doi:10.1007/s11010-013-1660-4

Cited by 125 publications

(122 citation statements)

References 34 publications

Supporting

Mentioning

105

Contrasting

Order By: Relevance

“…5D). A previous study has demonstrated that adropin is detected at granular and Purkinje cells in the cerebellum (37). Unfortunately, we could not find a suitable antiadropin antibody to perform a similar immunohistochemical FIGURE 5.…”

Section: Discussionmentioning

confidence: 99%

Adropin Is a Brain Membrane-bound Protein Regulating Physical Activity via the NB-3/Notch Signaling Pathway in Mice

Wong

Wang²,

Lee³

et al. 2014

Journal of Biological Chemistry

101

View full text Add to dashboard Cite

Background:The mechanism of action of adropin on metabolism remains elusive. Results: Adropin is a plasma membrane protein that can bind to the brain-specific, non-canonical Notch1 ligand NB-3. Conclusion: Adropin regulates physical activity, motor coordination, and cerebellum development in mice via the NB-3/ Notch1 signaling pathway. Significance: Adropin is a highly conserved polypeptide that might also be important for cerebellum development in mammals.

show abstract

Section: Discussionmentioning

confidence: 99%

Adropin Is a Brain Membrane-bound Protein Regulating Physical Activity via the NB-3/Notch Signaling Pathway in Mice

Wong

Wang²,

Lee³

et al. 2014

Journal of Biological Chemistry

101

View full text Add to dashboard Cite

show abstract

“…However, the source of the exercise training-induced increase in serum adropin levels remains unclear. Adropin is expressed in vascular endothelial cells, as well as in brain, heart, kidney, liver, pancreas, skeletal muscle, and small intestine (2,32). An in vitro study showed that adropin treatment promotes NO production from the human umbilical vein endothelial cells in a time-dependent manner, mediated via phosphorylation of eNOS protein (20).…”

Section: Discussionmentioning

confidence: 99%

“…Adropin consists of 76 amino acids and is encoded by a gene, Energy Homeostasis Associated (Enho) (16), and expressed in multiple tissues, including the brain, heart, kidney, liver, pancreas, skeletal muscle, and small intestine (2,32). Circulating adropin level decreases with age (7).…”

mentioning

confidence: 99%

Aerobic exercise training-induced changes in serum adropin level are associated with reduced arterial stiffness in middle-aged and older adults

Fujie

Hasegawa

Sato

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Fujie S, Hasegawa N, Sato K, Fujita S, Sanada K, Hamaoka T, Iemitsu M. Aerobic exercise training-induced changes in serum adropin level are associated with reduced arterial stiffness in middle-aged and older adults. Am J Physiol Heart Circ Physiol 309: H1642-H1647, 2015. First published September 14, 2015; doi:10.1152/ajpheart.00338.2015.-Aging-induced arterial stiffening is reduced by aerobic exercise training, and elevated production of nitric oxide (NO) participates in this effect. Adropin is a regulator of endothelial NO synthase and NO release, and circulating adropin level decreases with age. However, the effect of habitual aerobic exercise on circulating adropin levels in healthy middleaged and older adults remains unclear. We sought to determine whether serum adropin level is associated with exercise training-induced changes in arterial stiffness. First, in a cross-sectional study, we investigated the association between serum adropin level and both arterial stiffness and cardiorespiratory fitness in 80 healthy middle-aged and older subjects (65.6 Ϯ 0.9 yr). Second, in an intervention study, we examined the effects of 8-wk aerobic exercise training on serum adropin level and arterial stiffness in 40 healthy middle-aged and older subjects (67.3 Ϯ 1.0 yr) divided into two groups: aerobic exercise training and sedentary controls. In the cross-sectional study, serum adropin level was negatively correlated with carotid ␤-stiffness (r ϭ Ϫ0.437, P Ͻ 0.001) and positively correlated with plasma NOx level (r ϭ 0.493, P Ͻ 0.001) and cardiorespiratory fitness (r ϭ 0.457, P Ͻ 0.001). Serum adropin levels were elevated after the 8-wk aerobic exercise training intervention, and training-induced changes in serum adropin level were correlated with traininginduced changes in carotid ␤-stiffness (r ϭ Ϫ0.399, P Ͻ 0.05) and plasma NOx level (r ϭ 0.623, P Ͻ 0.001). Thus the increase in adropin may participate in the exercise-induced reduction of arterial stiffness. ARTERIAL STIFFNESS increases with age (26) owing to declines in endothelial function and autonomic function and increases in arterial wall thickness and calcification (1,3,4,11,18,24,26,31). This functional deterioration impairs the conduit and buffering functions of arteries, leading to several pathological conditions, including hypertension, atherosclerosis, and stroke (1,4,18,26). A cross-sectional study revealed that arterial stiffness was lower in individuals with higher levels of cardiorespiratory fitness (23, 28). Furthermore, habitual aerobic exercise reduces arterial stiffness (10, 28).Adropin consists of 76 amino acids and is encoded by a gene, Energy Homeostasis Associated (Enho) (16), and expressed in multiple tissues, including the brain, heart, kidney, liver, pancreas, skeletal muscle, and small intestine (2, 32). Circulating adropin level decreases with age (7). Recent work showed that adropin is expressed in vascular endothelial cells and promotes nitric oxide (NO) release by regulating endothelial nitric oxide synthase (eNOS) expression via vascul...

show abstract

“…However, all these studies are not specific to the cerebellum. Research studies related to the cerebellum are very few to our knowledge (1,2,4,7,8).…”

Section: Discussionmentioning

confidence: 99%

Analysis of diabetes-related cerebellar changes in streptozotocin-induced diabetic rats

Özdemir¹,

Akbaş²,

Kotil³

et al. 2016

Turk J Med Sci

View full text Add to dashboard Cite

IntroductionDiabetes mellitus (DM) comprises a group of common metabolic disorders that share the phenotype of hyperglycemia, leading to damage in a number of tissues. Retinas, neurons, and kidneys are especially affected (1). Acute and chronic complications may occur. Chronic complications are divided into vascular and nonvascular complications. Vascular complications are subdivided into microvascular (retinopathy, neuropathy, nephropathy) and macrovascular complications (coronary artery disease, peripheral vascular disease, cerebrovascular disease). Oxidative stress, glycosylation, and protein kinase-C activation are shown in all tissues affected by microvascular complications (1-3). Glucose homeostasis in humans is important for the functioning of the nervous system. The brain is an insulin-sensitive organ with widespread and selective expression of the insulin receptor in the olfactory bulb, hypothalamus, hippocampus, amygdala, cerebral cortex, and cerebellum; hypoglycemia and hyperglycemia affect the central and peripheral nervous system, leading to severe dysfunction (1-3).Chronic hyperglycemia is associated with functional and structural blood-brain barrier (BBB) changes in cerebral microvessels (3). Diabetes is also associated with gradually developing end-organ damage in the central nervous system, known as diabetic encephalopathy, characterized by impairment of cognitive functions and electrophysiological changes. Chronically increased intracellular glucose concentration leads to functional, structural, and neurodegenerative changes (1).Studies performing biochemical and structural analysis of the brain relevant to the ultrastructural features of diabetes are limited, and the number of cerebellar studies are even more so. This study aimed to analyze the structural and ultrastructural cerebellar changes in streptozotocin (STZ)-induced diabetic rats (2,4-6). Materials and methodsTwenty male adult Sprague Dawley rats weighing 200-220 g were obtained from the Experimental Medicine Research Institute (DETAE). Fourteen of these animals were selected as the diabetic group, and after 12 h of Background/aim: Diabetic peripheral neuropathy has been extensively studied and reported, but the number of studies that have investigated diabetes-related changes in the central nervous system are limited, with even fewer studies on the cerebellum. The aim of this experimental study was to perform a histologic analysis of the diabetes-related changes in the cerebellums of diabetic rats.Materials and methods: Twenty Sprague Dawley rats weighing between 200 and 220 g were included in the study. Diabetes was induced in 14 of these rats by a single intraperitoneal injection of 65 mg/kg streptozotocin dissolved in saline, while 6 animals constituted the control group. The induction of diabetes was confirmed by measuring the blood glucose levels in the tail blood with a glucometer. Levels equal to or above 200 mg/dL were considered diabetic. Induction of diabetes failed in 3 animals, who were then excluded from the study.Results...

show abstract

Expression of adropin in rat brain, cerebellum, kidneys, heart, liver, and pancreas in streptozotocin-induced diabetes

Cited by 125 publications

References 34 publications

Adropin Is a Brain Membrane-bound Protein Regulating Physical Activity via the NB-3/Notch Signaling Pathway in Mice

Adropin Is a Brain Membrane-bound Protein Regulating Physical Activity via the NB-3/Notch Signaling Pathway in Mice

Aerobic exercise training-induced changes in serum adropin level are associated with reduced arterial stiffness in middle-aged and older adults

Analysis of diabetes-related cerebellar changes in streptozotocin-induced diabetic rats

Contact Info

Product

Resources

About