Enhanced effect of daytime restricted feeding on the circadian rhythm of streptozotocin-induced type 2 diabetic rats

2012 ◽  
Vol 302 (9) ◽  
pp. E1027-E1035 ◽  
Author(s):  
Tao Wu ◽  
Fen ZhuGe ◽  
Lu Sun ◽  
Yinhua Ni ◽  
Ou Fu ◽  
...  

There is increasing awareness of the link between impaired circadian clocks and multiple metabolic diseases. However, the impairment of the circadian clock by type 2 diabetes has not been fully elucidated. To understand whether and how the function of circadian clock is impaired under the diabetic condition, we examined not only the expression of circadian genes in the heart and pineal gland but also the behavioral rhythm of type 2 diabetic and control rats in both the nighttime restricted feeding (NRF) and daytime restricted feeding (DRF) conditions. In the NRF condition, the circadian expression of clock genes in the heart and pineal gland was conserved in the diabetic rats, being similar to that in the control rats. DRF shifted the circadian phases of peripheral clock genes more efficiently in the diabetic rats than those in the control rats. Moreover, the activity rhythm of rats in the diabetic group was completely shifted from the dark phase to the light phase after 5 days of DRF treatment, whereas the activity rhythm of rats in the control group was still under the control of the suprachiasmatic nucleus (SCN) after the same DRF treatment. Furthermore, the serum glucose rhythm of type 2 diabetic rats was also shifted and controlled by the external feeding schedule, ignoring the SCN rhythm. Therefore, DRF shows stronger effect on the reentrainment of circadian rhythm in the type 2 diabetic rats, suggesting that the circadian system in diabetes is unstable and more easily shifted by feeding stimuli.

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Tianfei Hou ◽  
Wen Su ◽  
Ming Gong ◽  
Zhenheng Guo

Blood pressure (BP) exhibits 24-hour rhythm. Loss of BP oscillation has been found in up to 75% diabetic patients and is associated with increased risks of target organ injuries. However, the mechanisms underlying the disruption of BP circadian rhythm in diabetes remain poorly understood. We and others have demonstrated that type 2 diabetic db/db mice in C57/KsJ background have hypertension and severely disrupted BP circadian rhythm. Since these db/db mice were severely hyperglycemic (>600 mg/dL) as well as obese, it is unclear which factor or both contribute to the disruption of BP oscillation. Moreover, it is unclear whether clock genes are involved in the diabetes associated disruption of BP circadian rhythm. To address these specific questions, we cross bred the leptin receptor mutated db/db mice in the C57BL/KsJ background with PERIOD2::LUCIFERASE knock in mice in C57BL/6J background. At 4-5 months old, the blood glucose in these db/db -Per2 mice was higher than controls (320.3 vs 153 mg/dL) but was significantly lower than the C57/KsJ - db/db mice (608.5 mg/dL). However, the body weight of these db/db -per2 mice was significantly higher than both the C57/KsJ- db/db (66.4 vs 44.8 g) as well as control mice (33.9 g). The metabolic flexibility, which is represented by respiratory exchange ratio and measured using TSE LabMaster Indirect Calorimetry System, was significantly compromised in the db/db -per2 mice when compared to controls. We then determined the BP in the db/db -per2 mice using radiotelemetry under 12: 12 light: dark cycle. The circadian parameters of BP, including period length, amplitude and acrophase were calculated using Chronos-fit software. The results demonstrated that db/db -per2 mice have normal BP value but disrupted BP circadian rhythm, with decreased power of 24h oscillation, diminished amplitude and shifted acrophase. However, the extent of the disruption was significantly less than that we have reported in the C57/KsJ- db/db mice. By using LumiCycle, we are currently investigating the clock gene functions in various tissues including SCN, aorta, liver, and etc isolated from db/db -Per2 mice. In summary, we demonstrated that both hyperglycemia and obesity significantly contribute to the disruption in BP circadian rhythm in db/db mice.


2020 ◽  
Vol 21 (3) ◽  
pp. 831 ◽  
Author(s):  
Xiaoyue Pan ◽  
Meredith J. Taylor ◽  
Emma Cohen ◽  
Nazeeh Hanna ◽  
Samantha Mota

The goal of this review was to seek a better understanding of the function and differential expression of circadian clock genes during the reproductive process. Through a discussion of how the circadian clock is involved in these steps, the identification of new clinical targets for sleep disorder-related diseases, such as reproductive failure, will be elucidated. Here, we focus on recent research findings regarding circadian clock regulation within the reproductive system, shedding new light on circadian rhythm-related problems in women. Discussions on the roles that circadian clock plays in these reproductive processes will help identify new clinical targets for such sleep disorder-related diseases.


2020 ◽  
Vol 18 ◽  
pp. 205873922092915
Author(s):  
Dezhan Li ◽  
Wei Huang ◽  
Fang Yang ◽  
Bin Li ◽  
Shanshan Cai

Hypoxic–ischemic encephalopathy (HIE) in neonates can lead to severe chronic neurological deficit, including mental retardation, epilepsy, and sleep–wake cycle (SWC) disorder. Among these defects, little is known about the molecular mechanism of circadian rhythm disorder after HIE. Therefore, further study of sleep problems and its mechanism in HIE children will provide new ideas for clinical treatment of HIE children. For pediatric patients with cerebral ischemia, somnipathy often occurs due to visual and airway abnormalities. From May 2010 to August 2013, 128 newborns with history of HIE were followed up. Meanwhile, 88 normal full-term newborns in the same period were taken as the control group. The clinical data of the patients were collected and the sleep status was assessed by questionnaire. To establish the hypoxic–ischemic brain injury model of neonatal rats and analyze the mechanism of mir-182 in the circadian rhythm disorder caused by pineal function injury. The core clock genes during the regulation of the circadian clock were explored by bioinformatics methods. Patients’ sleep quality was affected by the circadian rhythm and respiratory problems; the pineal gland can regulate the core clock genes in the circadian clock during regulation. miR-182 was highly expressed in the pineal gland after hypoxic–ischemic brain damage (HIBD). Children with mild and moderate HIE showed significant sleep disorders in varying degrees, which provided a clinical basis for improving the long-term prognosis of children with HIE through targeted treatment of sleep disorders. MiR-182 is highly expressed in the pineal gland and is related to the expression of CLOCK protein. CLOCK gene is the target gene of miR-182, which provides a new target for the treatment of rhythm disorder related to the damage of pineal function caused by HIBD.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 643-P ◽  
Author(s):  
YANFEI HAN ◽  
LINDONG LI ◽  
YANJUN LIU ◽  
YOU WANG ◽  
CHUNHUA YAN ◽  
...  

2019 ◽  
Vol 82 (5) ◽  
pp. 56-63
Author(s):  
Abdulhadi Mohammad ◽  
◽  
I. Mikheitseva ◽  
S. Kolomiichuk ◽  
◽  
...  

2010 ◽  
Vol 8 (4) ◽  
pp. 293-297 ◽  
Author(s):  
Teng GUAN ◽  
Yi-Song QIAN ◽  
Meng-Hao HUANG ◽  
Long-Fei HUANG ◽  
Xu-Zhen TANG ◽  
...  

2020 ◽  
Vol 20 (3) ◽  
pp. 464-478 ◽  
Author(s):  
Yomna M. Yehya ◽  
Abdelaziz M. Hussein ◽  
Khaled Ezam ◽  
Elsayed A. Eid ◽  
Eman M. Ibrahim ◽  
...  

Objectives:: The present study was designed to investigate the effects of renin angiotensin system (RAS) blockade on cardiac arrhythmias and sympathetic nerve remodelling in heart tissues of type 2 diabetic rats. Methods:: Thirty-two male Sprague Dawley rats were randomly allocated into 4 equal groups; a) normal control group: normal rats, b) DM group; after type 2 diabetes induction, rats received 2ml oral saline daily for 4 weeks, c) DM+ ACEi: after type 2 diabetes induction, rats were treated with enalapril (10 mg/kg, orally for 4 weeks) and d) DM+ ARBs: after type 2 diabetes induction, rats were treated with losartan (30 mg/kg, orally for 4 weeks). Results:: In type 2 diabetic rats, the results demonstrated significant prolongation in Q-T interval and elevation of blood sugar, HOMA-IR index, TC, TGs, LDL, serum CK-MB, myocardial damage, myocardial MDA, myocardial norepinephrine and tyrosine hydroxylase (TH) density with significant reduction in serum HDL, serum insulin and myocardial GSH and CAT. On the other hand, blockade of RAS at the level of either ACE by enalapril or angiotensin (Ag) receptors by losartan resulted in significant improvement in ECG parameters (Q-T), cardiac enzymes (CK-MB), cardiac morphology, myocardial oxidative stress (low MDA, high CAT and GSH) and myocardial TH density. Conclusions:: RAS plays a role in the cardiac sympathetic nerve sprouting and cardiac arrhythmias induced by type 2 DM and its blockade might have a cardioprotective effect via attenuation of sympathetic nerve fibres remodelling, myocardial norepinephrine contents and oxidative stress.


2020 ◽  
Vol 20 (7) ◽  
pp. 1117-1132
Author(s):  
Abdelaziz M. Hussein ◽  
Elsayed A. Eid ◽  
Ismaeel Bin-Jaliah ◽  
Medhat Taha ◽  
Lashin S. Lashin

Background and Aims: In the current work, we studied the effects of exercise and stevia rebaudiana (R) extracts on diabetic cardiomyopathy (DCM) in type 2 diabetic rats and their possible underlying mechanisms. Methods: : Thirty-two male Sprague Dawley rats were randomly allocated into 4 equal groups; a) normal control group, b) DM group, type 2 diabetic rats received 2 ml oral saline daily for 4 weeks, c) DM+ Exercise, type 2 diabetic rats were treated with exercise for 4 weeks and d) DM+ stevia R extracts: type 2 diabetic rats received methanolic stevia R extracts. By the end of the experiment, serum blood glucose, HOMA-IR, insulin and cardiac enzymes (LDH, CK-MB), cardiac histopathology, oxidative stress markers (MDA, GSH and CAT), myocardial fibrosis by Masson trichrome, the expression of p53, caspase-3, α-SMA and tyrosine hydroxylase (TH) by immunostaining in myocardial tissues were measured. Results: T2DM caused a significant increase in blood glucose, HOMA-IR index, serum CK-MB and LDH, myocardial damage and fibrosis, myocardial MDA, myocardial α-SMA, p53, caspase-3, Nrf2 and TH density with a significant decrease in serum insulin and myocardial GSH and CAT (p< 0.05). On the other hand, treatment with either exercise or stevia R extracts significantly improved all studied parameters (p< 0.05). Moreover, the effects of stevia R was more significant than exercise (p< 0.05). Conclusion: Both exercise and methanolic stevia R extracts showed cardioprotective effects against DCM and Stevia R offered more cardioprotective than exercise. This cardioprotective effect of these lines of treatment might be due to attenuation of oxidative stress, apoptosis, sympathetic nerve density and fibrosis and upregulation of the antioxidant transcription factor, Nrf2.


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