Chrononutrition in the context of Ramadan: Potential implications.

Every year, healthy adult Muslims practice dawn to sunset fasting for a whole lunar month. No food or fluid is allowed for the fasting time window. After sunset, eating is allowed.

Ramadan Fasting and Changes in Thyroid Function in Hypothyroidism: Identifying Patients at Risk.

Ramadan fasting (RF) is associated with major changes in meal times. This can affect thyroxine absorption and thyroid function (TF) in patients with hypothyroidism. We aimed to examine the short- and long-term impact of RF on TF in patients with primary hypothyroidism on levothyroxine.

Weight and Glycemic Control Outcomes of Bariatric Surgery and Pharmacotherapy in Patients With Melanocortin-4 Receptor Deficiency.

Background: Melanocortin-4 receptor () mutations are the most common of the rare monogenic forms of obesity. However, the efficacy of bariatric surgery (BS) and pharmacotherapy on weight and glycemic control in individuals with MC4R deficiency (MC4R-d) is not well-established. We investigated and compared the outcomes of BS and pharmacotherapy in patients with and without MC4R-d.

Diabetes and Ramadan: Practical guidelines 2021.

Fasting during Ramadan is one of the five pillars of Islam and is obligatory for all healthy Muslims from the age of puberty. Though individuals with some illness and serious medical conditions, including some people with diabetes, can be exempted from fasting, many will fast anyway. It is of paramount importance that people with diabetes that fast are given the appropriate guidance and receive proper care.

Alterations in β-Cell Sphingolipid Profile Associated with ER Stress and iPLAβ: Another Contributor to β-Cell Apoptosis in Type 1 Diabetes.

Type 1 diabetes (T1D) development, in part, is due to ER stress-induced β-cell apoptosis. Activation of the Ca-independent phospholipase A beta (iPLAβ) leads to the generation of pro-inflammatory eicosanoids, which contribute to β-cell death and T1D. ER stress induces iPLAβ-mediated generation of pro-apoptotic ceramides via neutral sphingomyelinase (NSMase).

Ramadan fasting in insulin-treated patients is associated with potentially unfavourable changes in glucose metrics: A flash glucose monitoring (FGM) study.

Aim(s): Ramadan fasting (RF) can represent various challenges to glycaemic control especially in insulin-treated patients with diabetes. We aimed to assess the effect of RF on several glucose metrics using flash glucose monitoring (FGM).

Methods: Complete FGM data for 29-30 days before, during and after Ramadan were available for 40 patients with type 1 (n = 13) and type 2 diabetes (n = 27) on insulin (with or without oral hypoglycaemic) treatment.

Sphingolipid Metabolism in Glioblastoma and Metastatic Brain Tumors: A Review of Sphingomyelinases and Sphingosine-1-Phosphate.

Glioblastoma (GBM) is a primary malignant brain tumor with a dismal prognosis, partially due to our inability to completely remove and kill all GBM cells. Rapid tumor recurrence contributes to a median survival of only 15 months with the current standard of care which includes maximal surgical resection, radiation, and temozolomide (TMZ), a blood-brain barrier (BBB) penetrant chemotherapy. Radiation and TMZ cause sphingomyelinases (SMase) to hydrolyze sphingomyelins to generate ceramides, which induce apoptosis.

Diabetes and Ramadan: Utility of flash-glucose monitoring derived markers of glycaemic control and comparison with glycosylated haemoglobin.

Aims: Flash glucose monitoring (FGM)-derived markers of glucose control and variability and laboratory measured HbA1c among patients with diabetes on insulin in context of Ramadan fasting (RF) were examined and compared.

Methods: FGM data on insulin-treated patients (n = 20, age 42.3 ± 11.

Energy Metabolism and Intermittent Fasting: The Ramadan Perspective.

Intermittent fasting (IF) has been gaining popularity as a means of losing weight. The Ramadan fast (RF) is a form of IF practiced by millions of adult Muslims globally for a whole lunar month every year. It entails a major shift from normal eating patterns to exclusive nocturnal eating.

Calcium-independent phospholipases A2 and their roles in biological processes and diseases.

Among the family of phospholipases A2 (PLA2s) are the Ca(2+)-independent PLA2s (iPLA2s) and they are designated group VI iPLA2s. In relation to secretory and cytosolic PLA2s, the iPLA2s are more recently described and details of their expression and roles in biological functions are rapidly emerging. The iPLA2s or patatin-like phospholipases (PNPLAs) are intracellular enzymes that do not require Ca(2+) for activity, and contain lipase (GXSXG) and nucleotide-binding (GXGXXG) consensus sequences.

Inhibition of Ca2+-independent phospholipase A2β (iPLA2β) ameliorates islet infiltration and incidence of diabetes in NOD mice.

Autoimmune β-cell death leads to type 1 diabetes, and with findings that Ca(2+)-independent phospholipase A2β (iPLA2β) activation contributes to β-cell death, we assessed the effects of iPLA2β inhibition on diabetes development. Administration of FKGK18, a reversible iPLA2β inhibitor, to NOD female mice significantly reduced diabetes incidence in association with 1) reduced insulitis, reflected by reductions in CD4(+) T cells and B cells; 2) improved glucose homeostasis; 3) higher circulating insulin; and 4) β-cell preservation. Furthermore, FKGK18 inhibited production of tumor necrosis factor-α (TNF-α) from CD4(+) T cells and antibodies from B cells, suggesting modulation of immune cell responses by iPLA2β-derived products.

Evidence of contribution of iPLA2β-mediated events during islet β-cell apoptosis due to proinflammatory cytokines suggests a role for iPLA2β in T1D development.

Type 1 diabetes (T1D) results from autoimmune destruction of islet β-cells, but the underlying mechanisms that contribute to this process are incompletely understood, especially the role of lipid signals generated by β-cells. Proinflammatory cytokines induce ER stress in β-cells and we previously found that the Ca(2+)-independent phospholipase A2β (iPLA2β) participates in ER stress-induced β-cell apoptosis. In view of reports of elevated iPLA2β in T1D, we examined if iPLA2β participates in cytokine-mediated islet β-cell apoptosis.

Characterization of FKGK18 as inhibitor of group VIA Ca2+-independent phospholipase A2 (iPLA2β): candidate drug for preventing beta-cell apoptosis and diabetes.

Ongoing studies suggest an important role for iPLA2β in a multitude of biological processes and it has been implicated in neurodegenerative, skeletal and vascular smooth muscle disorders, bone formation, and cardiac arrhythmias. Thus, identifying an iPLA2βinhibitor that can be reliably and safely used in vivo is warranted. Currently, the mechanism-based inhibitor bromoenol lactone (BEL) is the most widely used to discern the role of iPLA2β in biological processes.

Genetic modulation of islet β-cell iPLA₂β expression provides evidence for its impact on β-cell apoptosis and autophagy.

β-cell apoptosis is a significant contributor to β-cell dysfunction in diabetes and ER stress is among the factors that contributes to β-cell death. We previously identified that the Ca²⁺-independent phospholipase A₂β (iPLA₂β), which in islets is localized in β-cells, participates in ER stress-induced β-cell apoptosis. Here, direct assessment of iPLA₂β role was made using β-cell-specific iPLA₂β overexpressing (RIP-iPLA₂β-Tg) and globally iPLA₂β-deficient (iPLA₂β-KO) mice.

Tumor suppressor Pdcd4 is a major transcript that is upregulated during in vivo pancreatic islet neogenesis and is expressed in both beta-cell and ductal cell lines.

Objectives: We wished to identify a major transcript that is upregulated during in vivo pancreatic islet neogenesis and examine the expression of the gene in beta and ductal cells.

Methods: Differential display polymerase chain reaction was used to identify upregulated transcripts after islet neogenesis was stimulated in the rat by brief occlusion of the main pancreatic duct. The expression of this major transcript, namely PDCD4 (programmed cell death gene 4), was measured in beta and ductal cells after stimulation with the incretin hormone glucagon-like peptide 1, mitogenic insulin, the thiazolidinedione rosiglitazone, and by high glucose concentrations.

Selenium stimulates pancreatic beta-cell gene expression and enhances islet function.

The present study investigated the role of selenium in the regulation of pancreatic beta-cell function. Utilising the mouse beta-cell line Min6, we have shown that selenium specifically upregulates Ipf1 (insulin promoter factor 1) gene expression, activating the -2715 to -1960 section of the Ipf1 gene promoter. Selenium increased both Ipf1 and insulin mRNA levels in Min6 cells and stimulated increases in insulin content and insulin secretion in isolated primary rat islets of Langerhans.