Relationships Between Changes in Serum Ketone Body Levels and Metabolic Effects in Patients with Severe Obesity Who Underwent Laparoscopic Sleeve Gastrectomy.

BACKGROUND: Serum ketone bodies increase due to dynamic changes in the lipid metabolisms of patients undergoing bariatric surgery. However, there have been few studies on the role of ketone bodies after bariatric surgery. We aimed to clarify the role of and relationship between the changes in serum ketone bodies and weight loss, as well as between those changes and the metabolic effects after laparoscopic sleeve gastrectomy (LSG). METHODS: We recruited 52 patients with severe obesity who underwent LSG. We measured acetoacetic acid (AcAc) and ß-hydroxybutyric acid (ß-OHB) at the baseline, 1 month, and 6 months after LSG. Subsequently, we compared the changes in the serum ketone bodies with weight-loss effects and various metabolic parameters. RESULTS: At 1 month after LSG, ß-OHB significantly increased (p = 0.009), then significantly decreased 6 months after LSG (p = 0.002). In addition, ß-OHB in patients without Type 2 diabetes (T2D) and metabolic dysfunction-associated steatohepatitis (MASH) was notably higher than in patients with T2D at 1 month after LSG (p < 0.001). In the early phase, both AcAc and ß-OHB mainly had strong positive correlations with changes in T2D- and MASH-related parameters. In the middle term after LSG, changes in both AcAc and ß-OHB were positively correlated with changes in lipid parameters and chronic kidney disease-related parameters. CONCLUSION: We demonstrated that the postoperative surge of ketone bodies plays a crucial function in controlling metabolic effects after LSG. These findings suggest the cause- and consequence-related roles of ketone bodies in the metabolic benefits of bariatric surgery.

Biceps femoris long head stiffens after 2 weeks of training cessation in highly trained sprinters.

PURPOSE: Most athletes experience short-term training cessation because of illness, injury, post-season vacation, or other reasons. Passive muscle stiffness is a potential risk factor for a sprint-type hamstring strain injury, but limited information is available about the effect of short-term training cessation on passive muscle stiffness. The present study aimed to identify whether and how passive muscle stiffness of the biceps femoris long head (BFlh) would vary due to 2 weeks of training cessation in sprinters. METHODS: Passive BFlh shear-wave speed (a proxy for stiffness) was measured using ultrasound shear-wave elastography in 28 male sprinters, before and after 2 weeks of intervention. During the 2 weeks, the participants in the training-cessation group (n = 14) were allowed to maintain their normal daily activities but not to perform any physical training, including stretching and resistance exercises. The participants in the training continuation group (n = 14) performed the training (including maximum speed sprint, plyometric, and weight training) prescribed by their coaches 5 days per week. RESULTS: In the training-cessation group, passive BFlh shear-wave speed increased after the 2 weeks of training cessation (4.75 ± 0.77 to 5.00 ± 0.88 m/s, P < 0.001). In contrast, there was no significant difference before and after the 2 weeks of training continuation (4.90 ± 0.85 to 4.93 ± 0.85 m/s, P = 0.521). CONCLUSIONS: The present findings indicate that muscles stiffen by training cessation in sprinting athletes.

Determining the structure of protein-bound ceramides, essential lipids for skin barrier function.

Protein-bound ceramides, specialized ceramides covalently bound to corneocyte surface proteins, are essential for skin permeability barrier function. However, their exact structure and target amino acid residues are unknown. Here, we found that epoxy-enone (EE) ceramides, precursors of protein-bound ceramides, as well as their synthetic analog, formed stable conjugates only with Cys among nucleophilic amino acids. NMR spectroscopy revealed that the ß-carbon of the enone was attached by the thiol group of Cys via a Michael addition reaction. We confirmed the presence of Cys-bound EE ceramides in mouse epidermis by mass spectrometry analysis of protease-digested epidermis samples. EE ceramides were reversibly released from protein-bound ceramides via sulfoxide elimination. We found that protein-bound ceramides with reversible release properties accounted for approximately 60% of total protein-bound ceramides, indicating that Cys-bound EE ceramides are the predominant protein-bound ceramides. Our findings provide clues to the molecular mechanism of skin barrier formation by protein-bound ceramides.