Obesity is a multifactorial disease linked to many comorbidities and has an impact on brain health. It is also known that obesity disrupts the endocannabinoid (eCB) system in the central nervous system and in the periphery, which complicates the underlying mechanisms behind obesity. However, weight loss through lifestyle interventions or bariatric surgery may alleviate obesity-related comorbidities, as well as restore eCB tone. Several studies have reported a decrease in circulating eCBs following weight loss, likely due to the positive association of these mediators with fat mass. However, further research is needed to clarify whether this reduction is a consequence of weight loss or plays a role in facilitating it. This review explores changes in circulating eCBs following weight loss and their potential roles in cerebral homeostasis and the reward system. It examines how lifestyle modifications and bariatric surgery may influence central eCB signalling and contribute to long-term weight loss success. Understanding the mechanisms behind improved brain function after weight loss could provide insights into optimizing obesity treatments.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly emerging as a global health crisis, affecting over 30% of the population and demanding urgent attention. This redefined condition, previously known as non-alcoholic fatty liver disease (NAFLD), reflects a deeper understanding of the intricate interplay between metabolic dysfunction and liver health. At the heart of MASLD lies the troubling accumulation of triglycerides (TGs) in hepatocytes, which precipitates insulin resistance and oxidative stress, ultimately leading to more severe forms like metabolic dysfunction-associated steatohepatitis (MASH). Excitingly, recent research has spotlighted the farnesoid X receptor (FXR) as a groundbreaking therapeutic target. FXR not only regulates lipid metabolism but also combats inflammation and insulin resistance, making it a potential game-changer in the fight against MASLD. With only one FDA-approved drug, resmetirom, currently available, the exploration of FXR agonists opens new avenues for innovative treatments that could revolutionize patient care. By harnessing the power of FXR to restore metabolic balance and integrating advanced strategies like lipidomics and fatty acid profiling, we stand on the brink of transforming how we approach MASLD and its associated complications, paving the way for a healthier future. This review delves into the promising role of FXR in combating MASLD and its implications for related metabolic disorders, emphasizing the urgency for advanced strategies to detect and manage this burgeoning epidemic.

Aim: Current diabetes guidelines recommend people with gestational diabetes mellitus (PwGDM) use primarily blood glucose meters (BGM) for diabetes management. We evaluated glycemic trends and guideline-recommended glycemic targets achieved in PwGDM using a diabetes app with a family of Bluetooth® connected BGMs. Methods: Anonymized glucose and app analytics data from 26,382 PwGDM were sourced from a server. Data from their first 7-days using the app with connected BGMs was compared to 7-days prior to a 10-week timepoint. Results: Percent fasting readings in range (RIR, < 5.3 mmol/L) improved by +20.3 percentage points in the overall population. Improved glucose RIR (3.5 to 7.8 mmol/L) (+8.3 percentage points), mean blood glucose (BG, –0.59 mmol/L), and fasting RIR (+33.2 percentage points) were observed in those with baseline mean BG ≥ 6.1 mmol/L. Improvements in mean BG of –0.32 to –2.36 mmol/L, and RIR of +3.0 to +38.3 percentage points correlated with higher baseline mean BG ≥ 6.1 to ≥ 7.8 mmol/L. Only 58.5% of PwGDM with baseline mean BG ≥ 6.1 mmol/L had > 80% RIR at baseline, which improved to 79.5% at 10 weeks. PwGDM averaged 17 app sessions and 90 minutes per week on the app. Conclusions: PwGDM engaged with the diabetes app and connected BGM, facilitating attainment of glycemic targets, an especially important outcome for those with higher mean glucose at baseline.