Disturbance of regulation of NO synthase activity by peptides of insulin family in rat skeletal muscles in streptozotocin model of neonatal type 2 diabetes mellitus

Kuznetsova, L. A.; Chistyakova, O. V.; Бондарева, В. М.; Sharova, T. S.; Pertseva, M. N.

doi:10.1134/s1607672910030087

Cited by 3 publications

(2 citation statements)

References 11 publications

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“…NO regulates various biological processes, and is produced by NO synthase (Stamler & Meissner, ). There are data that indicate relaxin stimulates NO synthase signaling in the skeletal muscles of type 2 diabetic rats, leading to NO dysfunction (Kuznetsova et al., ).…”

Section: Musclementioning

confidence: 99%

The effect of relaxin on the musculoskeletal system

Dehghan

Haerian

Muniandy

et al. 2013

Scandinavian Med Sci Sports

120

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Relaxin is a hormone structurally related to insulin and insulin-like growth factor, which exerts its regulatory effect on the musculoskeletal and other systems through binding to its receptor in various tissues, mediated by different signaling pathways. Relaxin alters the properties of cartilage and tendon by activating collagenase. This hormone is also involved in bone remodeling and healing of injured ligaments and skeletal muscle. In this review, we have summarized the literature on the effect of relaxin in musculoskeletal system to provide a broad perspective for future studies in this field.

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Section: Musclementioning

confidence: 99%

The effect of relaxin on the musculoskeletal system

Dehghan

Haerian

Muniandy

et al. 2013

Scandinavian Med Sci Sports

120

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“…After addition of either ALMi, grip strength and gait speed to the model there was enrichment for PKB/AKT signalling pathways, known to play a pivotal role in JNK, AMPK and insulin signalling pathways; this suggests that the epigenetic dysregulation of these pathways in insulin resistant individuals may in part be independent of muscle mass and strength. Interestingly, after adjustment for BMI, although there was still enrichment amongst insulin and JNK signalling pathways, there was also enrichment amongst epidermal growth factor (EGFR) and relaxin signalling pathways suggesting potential effects of IR independent of body composition on muscle stem cell activation, differentiation and survival [ 53 – 55 ].…”

Section: Discussionmentioning

confidence: 99%

DNA methylation of insulin signaling pathways is associated with HOMA2-IR in primary myoblasts from older adults

Burton,

Garratt,

Hewitt

et al. 2023

Skeletal Muscle

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Background While ageing is associated with increased insulin resistance (IR), the molecular mechanisms underlying increased IR in the muscle, the primary organ for glucose clearance, have yet to be elucidated in older individuals. As epigenetic processes are suggested to contribute to the development of ageing-associated diseases, we investigated whether differential DNA methylation was associated with IR in human primary muscle stem cells (myoblasts) from community-dwelling older individuals. Methods We measured DNA methylation (Infinium HumanMethylationEPIC BeadChip) in myoblast cultures from vastus lateralis biopsies (119 males/females, mean age 78.24 years) from the Hertfordshire Sarcopenia Study extension (HSSe) and examined differentially methylated cytosine phosphate guanine (CpG) sites (dmCpG), regions (DMRs) and gene pathways associated with HOMA2-IR, an index for the assessment of insulin resistance, and levels of glycated hemoglobin HbA1c. Results Thirty-eight dmCpGs (false discovery rate (FDR) < 0.05) were associated with HOMA2-IR, with dmCpGs enriched in genes linked with JNK, AMPK and insulin signaling. The methylation signal associated with HOMA2-IR was attenuated after the addition of either BMI (6 dmCpGs), appendicular lean mass index (ALMi) (7 dmCpGs), grip strength (15 dmCpGs) or gait speed (23 dmCpGs) as covariates in the model. There were 8 DMRs (Stouffer < 0.05) associated with HOMA2-IR, including DMRs within T-box transcription factor (TBX1) and nuclear receptor subfamily-2 group F member-2 (NR2F2); the DMRs within TBX1 and NR2F2 remained associated with HOMA2-IR after adjustment for BMI, ALMi, grip strength or gait speed. Forty-nine dmCpGs and 21 DMRs were associated with HbA1c, with cg13451048, located within exoribonuclease family member 3 (ERI3) associated with both HOMA2-IR and HbA1c. HOMA2-IR and HbA1c were not associated with accelerated epigenetic ageing. Conclusions These findings suggest that insulin resistance is associated with differential DNA methylation in human primary myoblasts with both muscle mass and body composition making a significant contribution to the methylation changes associated with IR.

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Streptozotocin-Induced Diabetes Mellitus in Neonatal Rats: An Insight into its Applications to Induce Diabetic Complications

Mirza¹,

Panchal

2019

CDR

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Background: Diabetic complications are the major contributor in the mortality of diabetic patients despite controlling blood glucose level. In the journey of new drug discovery, animal models have to play a major role. A large number of chemical-induced and genetically modified animal models have been investigated to induce diabetic complications but none of them was found to be mimicking the pathophysiology of the human. Therefore, the search and identification of the appropriate animal model become essential. Objective: In the present review, we have made an attempt to understand the pathophysiology of diabetic complication in the neonatal streptozotocin-diabetic rat model and tried to identify the targets for therapeutic agents. The review will help the researchers to explore the animal model to induce diabetic complications, to identify targets and further to find lead molecules for treatment or prevention of diabetic complications. Methods: We have compiled the available research work from 1974 by using prominent databases, organized the available information and analyzed the data to improve the understanding of the pathophysiology of streptozotocin-induced diabetic complications in neonates of rats. Results: The neonatal streptozotocin-diabetic rat model is frequently used and well-established animal model for type 2 diabetes mellitus. We have found that this model has been used to study the pathogenesis of various micro and macrovascular diabetic complications and also investigated for its effects on the liver, thymus gland, and brain. The underlying pathophysiology for complications had a resemblance to the human. Conclusion: The neonatal streptozotocin-diabetic rat model may demonstrate symptomatic diabetic complications due to persistent hyperglycemia at the age of approximately 18-24 weeks. Critical interpretations of available research work showed that the researcher can explore split dose STZ (90- 100mg/kg b.w) model to induce Type 2 DM in neonates of rats at 2nd or 3rd postnatal day.

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Disturbance of regulation of NO synthase activity by peptides of insulin family in rat skeletal muscles in streptozotocin model of neonatal type 2 diabetes mellitus

Cited by 3 publications

References 11 publications

The effect of relaxin on the musculoskeletal system

The effect of relaxin on the musculoskeletal system

DNA methylation of insulin signaling pathways is associated with HOMA2-IR in primary myoblasts from older adults

Streptozotocin-Induced Diabetes Mellitus in Neonatal Rats: An Insight into its Applications to Induce Diabetic Complications

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