Melatonin oral gel(Spherium Biomed SL)

A recent case study reported a non-24 h sleep-wake disorder in a patient with myotonic dystrophy type 1 (DM1). Research on intrinsic circadian rhythm sleep-wake disorders (CRSWDs) in DM1 patients is though lacking. This study utilized actigraphy to ascertain the presence of CRSWDs in DM1 patients and establish a comparison with healthy control subjects.

Thirty-three patients with genetic diagnosis of DM1 and 33 age- and sex-matched healthy control subjects wore an actigraph and filled out a sleep diary for two consecutive weeks. Sleep, light exposure, and nonparametric measures were computed from actigraphic data.

DM1 patients exhibit poorer sleep quality and delayed sleep-wake episodes as well as reduced daylight exposure compared to healthy control subjects. Importantly, 3 DM1 patients (9.1 %) had a delayed sleep phase disorder and 3 DM1 patients had an irregular sleep-wake rhythm disorder (ISWRD) (9.1 %) whereas no control subject exhibited a CRSWD. DM1 patients with an ISWRD presented lower inter-daily stability (IS) (0.16 vs. 0.44, p < 0.05) and relative amplitude (RA) (0.36 vs. 0.79, p < 0.01) as well as higher intra-daily variability (IV) (1.22 vs. 0.79, p < 0.05) than DM1 patients with a normal sleep phenotype. DM1 patients with CRSWDs were more likely to exhibit excessive daytime sleepiness (EDS) than those with a normal sleep phenotype (83.3 % vs. 37.0 %, p < 0.05).

Core clinical implications are the need to systematically screen DM1 patients for CRSWDs and apply a multimodal chronotherapy (sleep hygiene, timed light, and melatonin). Recognizing and treating CRSWDs can help address significant sleep disturbances, like EDS.

Type 2 diabetes mellitus (T2DM), accounting for approximately 90% of adult-onset diabetes cases, is a major risk factor for diabetic kidney disease (DKD). Emerging evidence has linked T2DM with disrupted circadian rhythms. However, its role in the progression of DKD remains poorly understood. To investigate the relationship between circadian rhythms and DKD, we used the type 2 diabetic nephropathy (T2DN) rat, a non-obese model that replicates key features of human DKD. Circadian rhythms were assessed in both male and female T2DN rats at 20 and &gt;35 weeks (young and old) by continuous measurements of mean arterial pressure (MAP), systolic blood pressure (SBP), heart rate, and locomotor activity. Differential expression of circadian genes was evaluated by RNA sequencing of kidney cortex. In separate cohorts, the effects of renal denervation and melatonin treatment on circadian parameters were examined. T2DN rats exhibited impaired circadian rhythms in MAP and SBP, while heart rate and locomotor activity retained rhythmicity. Transcriptomic analysis revealed altered expression of several circadian-related genes, including core circadian gene Per1 and multiple circadian-controlled genes involved in insulin sensitivity, lipid metabolism, and immune regulation between different groups of T2DN rats. Neither renal denervation nor melatonin administration restored normal circadian rhythms of T2DN rats. Our data suggest that circadian rhythm disruption of blood pressure is a consistent feature of T2DN rats and that targeting circadian clock components such as Per1 could offer potential therapeutic strategies.