Ameliorative effect of astaxanthin on endothelial dysfunction in streptozotocin-induced diabetes in male rats

2011 ◽  
Vol 61 (04) ◽  
pp. 239-246 ◽  
Author(s):  
Zi-Wen Zhao ◽  
Wei Cai ◽  
Yun-Ling Lin ◽  
Qing-Fei Lin ◽  
Qiong Jiang ◽  
...  
Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4157-4167 ◽  
Author(s):  
Thomas H. Meek ◽  
Miles E. Matsen ◽  
Vincent Damian ◽  
Alex Cubelo ◽  
Streamson C. Chua ◽  
...  

Abstract Although the antidiabetic effects of leptin require intact neuronal melanocortin signaling in rodents with uncontrolled diabetes (uDM), increased melanocortin signaling is not sufficient to mimic leptin's glucose-lowering effects. The current studies were undertaken to clarify the role of melanocortin signaling in leptin's ability to correct metabolic and neuroendocrine disturbances associated with uDM. To accomplish this, bilateral cannulae were implanted in the lateral ventricle of rats with streptozotocin-induced diabetes, and leptin was coinfused with varying doses of the melanocortin 3/4 receptor (MC3/4R) antagonist, SHU9119. An additional cohort of streptozotocin-induced diabetes rats received intracerebroventricular administration of either the MC3/4R agonist, melanotan-II, or its vehicle. Consistent with previous findings, leptin's glucose-lowering effects were blocked by intracerebroventricular SHU9119. In contrast, leptin-mediated suppression of hyperglucagonemia involves both melanocortin dependent and independent mechanisms, and the degree of glucagon inhibition was associated with reduced plasma ketone body levels. Increased central nervous system melanocortin signaling alone fails to mimic leptin's ability to correct any of the metabolic or neuroendocrine disturbances associated with uDM. Moreover, the inability of increased melanocortin signaling to lower diabetic hyperglycemia does not appear to be secondary to release of the endogenous MC3/4R inverse agonist, Agouti-related peptide (AgRP), because AgRP knockout mice did not show increased susceptibility to the antidiabetic effects of increased MC3/4R signaling. Overall, these data suggest that 1) AgRP is not a major driver of diabetic hyperglycemia, 2) mechanisms independent of melanocortin signaling contribute to leptin's antidiabetic effects, and 3) melanocortin receptor blockade dissociates leptin's glucose-lowering effect from its action on other features of uDM, including reversal of hyperglucagonemia and ketosis, suggesting that brain control of ketosis, but not blood glucose levels, is glucagon dependent.


Andrologia ◽  
2021 ◽  
Author(s):  
Marzieh Pirzadeh ◽  
Mohammad Barary ◽  
Seyed Mohammad Hosseini ◽  
Sohrab Kazemi ◽  
Ali Akbar Moghadamnia

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 682
Author(s):  
Yasmina K. Mahmoud ◽  
Ahmed A. Ali ◽  
Heba M. A. Abdelrazek ◽  
Tahany Saleh Aldayel ◽  
Mohamed M. Abdel-Daim ◽  
...  

The ameliorative effect of L-arginine (LA) and L-carnitine (LC) against fipronil (FPN)-induced neurotoxicity was explored. In this case, 36 adult male rats were randomly divided into six groups: group I received distilled water, group II received 500 mg/kg LA, group III received 100 mg/kg LC, group IV received 4.85 mg/kg FPN, group V received 4.85 mg/kg FPN and 500 mg/kg LA and group VI received 4.85 mg/kg FPN and 100 mg/kg LC for 6 weeks. Cognitive performance was assessed using Barnes maze (BM). Serum corticosterone, brain total antioxidant capacity (TAC), malondialdehyde (MDA) and dopamine were measured. Histopathology and immunohistochemistry of ionized calcium-binding adaptor (Iba-1), doublecortin (DCX) and serotonin (S-2A) receptors were performed. Fipronil induced noticeable deterioration in spatial learning and memory performance. In addition, FPN significantly (p < 0.05) diminished brain antioxidant defense system and dopamine coincide with elevated serum corticosterone level. Histopathological examination revealed degenerative and necrotic changes. Furthermore, Iba-1 and DCX were significantly expressed in cortex and hippocampus whereas S-2A receptors were significantly lowered in FPN group. However, administration of LA or LC alleviated FPN-induced deteriorations. In conclusion, LA and LC could be prospective candidates for mitigation of FPN-induced neurotoxicity via their antioxidant, anti-inflammatory and neuropotentiating effects.


2020 ◽  
Vol 6 (1) ◽  
pp. 24
Author(s):  
Viani Anggi ◽  
Joni Tandi ◽  
Veronika Veronika

This study aims to determine the content of flavonoid and the effect of ethanol extract of moringa seeds on the regeneration of pancreatic β cells in male white rats streptozotocin induced diabetes. This study method used has total flavonoid equivalent quercetin by spectrophotometry uv-vis and to regeneration of pancreatic β cells in male white rats used 30 test animals,namely male white rats divided into 6 groups, each group consisted of 5 male white rats with details of group I as normal control, Group II as negative control given 0.5% Na-CMC suspension, Group III as positive control given glibenclamide suspension and in Groups IV, V, and VI were given with each dose of 100 mg/kg BW, 200 mg/kg BW and 400 mg/kg BB. Histopathological damage picture of the pancreas was observed by staining HE using a 400x magnification olympus Cx21 microscope. The results showed that the ethanol extract of moringa seeds contained secondary metabolites, namely flavonoids, alkaloids, saponins and tannins. The results showed has total flavonoid equivalent quercetin of moringa seeds is 1,26% and regeneration of pancreatic β cells in male white rats streptozotocin induced diabetes of Moringa seed ethanol extract at a dose of 400 mg/kg BB can have an effect on the regeneration of β cells in the pancreas of white diabetic male rats.  


2007 ◽  
Vol 10 (10) ◽  
pp. 1661-1666 ◽  
Author(s):  
Soleimani Safiyeh ◽  
Fathiazar Baijani Fathallah ◽  
Nejati Vahid ◽  
Nazemiyeh Hossine ◽  
Shojaei Sadee Habib

1984 ◽  
Vol 247 (3) ◽  
pp. G226-G230
Author(s):  
R. B. Kirkpatrick ◽  
B. G. Kraft

The sulfation of bile acids is hormone dependent, being increased in females and ethynylestradiol (EE)-treated males compared with normal males. Diabetes causes significant alterations in estrogen metabolism and uterine estrogen receptor kinetics. Male rats were given streptozotocin (90 mg/kg) and diabetes was verified. An increase in hepatic bile acid sulfotransferase (BAST) activity was significant by 6 days and continued to increase to 29 days. This increase was prevented by insulin replacement. Administration of EE (6.0-600 micrograms X kg-1 X day-1) to normal male rats resulted in a significant increase in hepatic BAST activity; however, administration of similar doses of EE to diabetic males failed to further increase activity levels over the already-elevated levels in the diabetic controls. This increase in in vitro specific activity was accompanied by an increase in the biliary excretion of lithocholate 3-sulfate and taurolithocholate 3-sulfate in 21-day-diabetic animals. Bile flow and total bile acid excretion were also markedly increased in the diabetic animals. The data indicate that streptozotocin-induced diabetes causes a significant increase in hepatic BAST activity. These findings are consistent with an alteration in hepatic estrogen action in streptozotocin-induced diabetes.


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