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Mechanistically, cherries exhibit relatively high antioxidant activity, low glycemic response, COX 1 and 2 enzyme inhibition, and other anti-carcinogenic effects in vitro and in animal experiments.
Cherries appear to aid in diabetes control and diminution of the complications of the disease.
Sour cherries supplementation in particular, has been reported to benefit in recovery from exercise-induced muscle damage.
Results of the present study suggest a selective modulatory effect of sweet cherries on CRP, NO, and RANTES.

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Why citric acid can holding carotenoid from oxidation?
5 answers
Citric acid can help prevent the oxidation of carotenoids due to its antioxidant properties. It acts as a quencher of singlet oxygen, which is a reactive oxygen species that can oxidize carotenoids. When carotenoids are oxidized, they can produce reactive carbonyl compounds that can lead to oxidative stress. However, the addition of citric acid can enhance the oxidative stability of carotenoids and improve their shelf life. Citric acid can also play a role in reducing oxidative damage in cells and improving the immune system. It has been shown to have antioxidant and anti-inflammatory actions, which can help protect the liver and brain. Additionally, citric acid can enhance the bioavailability of essential minerals like iron, which can help reduce anemia. Overall, citric acid's antioxidant properties and ability to reduce oxidative damage contribute to its ability to prevent carotenoid oxidation.
How does diabetes worsen with beta cell dysfunction?
3 answers
Diabetes worsens with beta cell dysfunction because beta cells are responsible for producing and secreting insulin, which helps regulate blood glucose levels. When beta cells become dysfunctional, they are unable to produce enough insulin, leading to elevated blood glucose levels. This dysfunction is observed in both type 1 and type 2 diabetes. In type 2 diabetes, beta cells initially adapt to insulin resistance by increasing insulin secretion, but over time, they become exhausted and their mass decreases. This decrease in beta cell mass and function contributes to the progression of diabetes and the worsening of glycemic control. It is important to preserve or recover beta cell functional mass in the management of type 2 diabetes, as beta cell regenerative capacity is limited in humans. Lifestyle modifications, such as weight loss and reducing beta cell workload, are effective strategies for preserving beta cell function and managing type 2 diabetes.
What changes happen in beta cells in t2dm?
5 answers
Beta cells in type 2 diabetes (T2DM) undergo changes in gene expression, reverting to a more immature state and in some cases transdifferentiating into other islet cell types. These changes are associated with alterations in β-cell identity and mass, as well as changes in metabolism and intracellular signaling. The defects in β-cells leading to T2DM vary among individuals and include variations in β-cell mass, development, expansion, responses to stress, insulin production and secretion, and intracellular signaling pathways. Some β-cells undergo dedifferentiation without dying in T2DM, suggesting potential strategies to revive these cells and restore their functionality.
How are beta cells involved in pathogenesis of type 2 diabetes?
5 answers
Beta cells are involved in the pathogenesis of type 2 diabetes through various mechanisms. One important factor is the downregulation of arginase 2 (ARG2) in human pancreatic beta cells, which regulates the synthesis of polyamines that are involved in beta cell function and pancreas development. Additionally, alpha cells within the islets of Langerhans play a significant role in glucose homeostasis and communicate with other cells through glucagon action, contributing to the bi-hormonal model of type 2 diabetes. Furthermore, beta cell dysfunction and reduced beta cell mass with aging are associated with the development of type 2 diabetes, suggesting a role for beta cell senescence in the pathogenesis of the disease. Insulin resistance, which is a major cause of type 2 diabetes, leads to elevated free fatty acid levels that can disrupt lipid metabolism and contribute to decreased beta cell function and lipotoxicity. Epigenetic modifications, such as DNA methylation, have also been found to play a significant role in the development of beta cell dysfunction in type 2 diabetes.
How do pancreatic beta cells secrete insulin?
3 answers
Pancreatic beta cells secrete insulin through a dynamic and highly regulated process. Insulin secretion is influenced by multiple regulatory layers that allow beta cells to adapt to changes in nutrient availability and metabolic demand. The process involves the regulation of histone modifications, which play a role in acute adaptations to fasting and feeding cycles. Cholesterol homeostasis also plays a crucial role in beta cell function, including early steps of insulin synthesis and secretion. Insulin secretion is triggered by an increase in intracellular ATP concentration, leading to the closure of KATP channels, depolarization of the cell, and opening of voltage-gated calcium channels. Insulin secretion occurs in a pulsatile manner, with oscillatory pulses superimposed on a basal secretion rate. Understanding the mechanisms of insulin secretion and the factors that regulate it is important for the development of therapeutic interventions for metabolic disorders such as diabetes.
Is GPR27 deorphanised?
4 answers
GPR27 is an orphan G protein-coupled receptor (GPCR) that has been studied in various contexts. In the context of energy metabolism, GPR27 has been found to play a role in lipid metabolism, insulin signaling, and glucose homeostasis. In pancreatic beta cells, GPR27 has been implicated in insulin transcription and glucose-stimulated insulin secretion. Additionally, GPR27 has been linked to insulin secretion in the central nervous system. In the context of hepatocellular carcinoma (HCC), GPR27 has been shown to affect the proliferation of HCC cells through the MAPK/ERK pathway. However, despite these findings, GPR27 remains an orphan receptor as no confirmed ligands have been identified for it.
What are methyl thiophanate effects on bone?
5 answers
Methyl thiophanate has been shown to induce severe mineral perturbations, including calcium and phosphorus levels, in plasma, urine, and bone. It also leads to increased lipid peroxidation and advanced oxidation protein products levels in erythrocytes and bone, along with a depletion of antioxidant status in both tissues. Additionally, methyl thiophanate treatment has been associated with DNA degradation and histological variation in bone and blood. However, another study found no direct relation between methyl thiophanate dosage levels and chromosomal breaks in bone marrow cells. It also did not exert significant mutagenic, cytogenic, and teratogenic effects on bone development in rats. Overall, the effects of methyl thiophanate on bone appear to be complex and may vary depending on the specific experimental conditions and species studied.
What does high albumin/creatinine indicate?
3 answers
High albumin/creatinine ratio (ACR) is an indicator of microvascular damage, renal disease, and kidney dysfunction. It has been linked to cardiovascular events, including stroke. A high ACR at admission may predict a poor outcome in patients with acute ischemic stroke. In a primary prevention population, a high-normal urine ACR (>6 mg/g) independently predicts an increased risk of mortality. The urine ACR is a reliable predictor of mortality and improves the predictive ability of traditional biomarkers and risk scores. A high ACR is associated with a higher risk of hypertension, type 2 diabetes, and stroke. It is also related to older age, lower high-density lipoprotein cholesterol level, higher total cholesterol level, higher systolic blood pressure, higher prevalence of current smoking, higher prevalence of diabetes, and higher anti-hypertensive medication use.
What are the challenges of psychiatrists in handling patients with psychological illness?
5 answers
Psychiatrists face several challenges in handling patients with psychological illness. One challenge is the time pressure they experience, which can hinder their ability to make a comprehensive formulation of the patient's illness. Additionally, some psychiatrists prioritize their medical role over the holistic approach to patient care, which can impact the quality of treatment provided. Another challenge is the management of ambiguity in diagnosis and patient management, as well as containing the anxiety experienced by patients and their families. Furthermore, psychiatrists may struggle with acknowledging treatment failure and may continue with futile treatment, prolonging patient suffering. It is important for psychiatrists to recognize the limitations of their scientific skills and consider end-of-life decisions when necessary. Overall, psychiatrists must navigate these challenges to ensure high clinical standards and provide the best possible care for patients with psychological illness.
Anti ulcerogenic properties of the unripe fruit of musa balbisiana colla?
4 answers
The unripe fruit of Musa balbisiana Colla has been found to possess anti-ulcerogenic properties. Studies have shown that the fruit extracts exhibit significant anti-ulcer activity in various models, including ethanol-induced stomach ulcer and acetic acid-induced ulcer models. The extracts have also demonstrated the ability to decrease ulcer parameters such as ulcer score and ulcer index in a dose-dependent manner. Additionally, the fruit extracts have been found to have anti-inflammatory activity and antibacterial activity against E. coli, P. aeruginosa, and S. aureus. These findings suggest that Musa balbisiana Colla fruit has potential as a natural remedy for ulcers and related conditions.
What are the side effects of metformin upon aerobic training?
3 answers
Metformin has been shown to have conflicting effects on the improvements in insulin sensitivity and cardiorespiratory fitness with aerobic training. In older adults, metformin was found to attenuate the increase in whole-body insulin sensitivity and VO2 max after aerobic exercise training (AET) by inhibiting skeletal muscle mitochondrial respiration and protein synthesis. However, in hyperglycemic individuals with metabolic syndrome (MetS), chronic metformin treatment did not affect fasting insulin sensitivity improvements with aerobic exercise training, although it did reduce the improvements in VO2 max. The exact side effects of metformin on aerobic training seem to vary depending on the population studied and the specific outcomes measured. Further research is needed to fully understand the mechanisms and potential negative effects of metformin on the benefits of aerobic training.