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Neurocognitive regression can be observed as the main neurological complications after CABG Vitamin D may help prevent neurodegeneration as it plays an important role in the regulation of neurotrophic factors, neurogenesis, In our study we aimed to evaluate whether the preoperative vitamin-D levels of patients who will undergo CABG surgery have an effect on postoperative neurocognitive functions Between May 2021 and November 2022, 100 patients with ASA 1-3 risk score, aged 18-70 who were scheduled for elective CABG surgery were included in the study. All patient were divided into 2 groups. While Vitamin D insufficiency group has 21-29 ng/ml serum 25(OH)D3 level, Vitamin D deficiency group has less than 20 ng/ml serum 25(OH)D3. Demographic characteristics of the patients, age, gender, BMI, educational status, comorbidities and medications, alcohol abuse, ASA classification, preoperative left ventricular ejection fraction value, preoperative 25 OH vitamin D level, NYHA (New York Heart Association Functional Classification) classification, EuroSCORE 2 values were recorded. MOCA cognitive assessment test was applied to the patients 1 day before the operation and 5-7 days after operation. NIRS monitoring was applied to the patients during the surgery. S100B and CXCL10 Ligand were measured preoperatively and at the postoperative 48th hour. The length of stay of the patients in the intensive care unit and hospital, APACHE2 score in the first 24 hours postoperatively and CASUS score for 5 days postoperatively were also calculated and recorded. 27 cases of POCD; Vitamin D deficiency was detected in 6 of them, and vitamin D deficiency was detected in the remaining 21. When the effect of vitamin D levels on the development of POCD was analyzed; POCD developed in 30% of patients with vitamin D deficiency and in 20% of patients with vitamin D insufficiency POCD developed in 30% of patients with vitamin D deficiency and in 20% of patients with vitamin D insufficiency. Although a higher rate of POCD was observed in patients with vitamin D deficiency.In 27 cases with POCD; mean MV adherence time length of stay in the intensive care unit [p=0.015], length of stay in the hospital were found to be significantly longer. No significant difference was found between cerebral desaturation and POCD development in NIRS monitoring. Median preop S100B values of all patients were 34.51 ,postoperative S100B values were 48.37 ,preop CXCL 10 values were 71.32 and postoperative CXCL 10 values were calculated as 89.33. Although both S100B and CXCL 10 values increased in the postoperative period compared to the preoperative period in all patients, no statistically significant increase was observed in those with vitamin D deficiency compared to the insufficiency (p>0.05). According to the analyzes performed, a negative correlation was found between the postoperative CXCL 10 value and the postoperative MOCA score (p<0.04) In patients who underwent isolated CABG surgery with vitamin D deficiency/deficiency; We have seen that POCD risk factors such as advanced age, HT, DM, especially in deficient ones, are compatible with the literature [ABSTRACT FROM AUTHOR]

Liver mitochondria undergo architectural remodeling that maintains energy homeostasis in response to feeding and fasting. However, the specific components and molecular mechanisms driving these changes and their impact on energy metabolism remain unclear. Through comparative mouse proteomics, we found that fasting induces strain-specific mitochondrial cristae formation in the liver by upregulating MIC19, a subunit of the MICOS complex. Enforced MIC19 expression in the liver promotes cristae formation, mitochondrial respiration, and fatty acid oxidation while suppressing gluconeogenesis. Mice overexpressing hepatic MIC19 show resistance to diet-induced obesity and improved glucose homeostasis. Interestingly, MIC19 overexpressing mice exhibit elevated energy expenditure and increased pedestrian locomotion. Metabolite profiling revealed that uracil accumulates in the livers of these mice due to increased uridine phosphorylase UPP2 activity. Furthermore, uracil-supplemented diet increases locomotion in wild-type mice. Thus, MIC19-induced mitochondrial cristae formation in the liver increases uracil as a signal to promote locomotion, with protective effects against diet-induced obesity. [Display omitted] • Fasting induces strain-specific cristae formation and MIC19 in liver mitochondria • MIC19 drives cristae formation in BL6 liver and protects against diet-induced obesity • Hepatic MIC19 promotes mitochondrial respiration and energy expenditure • MIC19 overexpression in the liver promotes pedestrian locomotion through uracil production Sohn et al. investigate how cristae formation in the liver is regulated upon nutritional changes and the effects of cristae on hepatic and whole-body energy metabolism. Hepatic MIC19 contributes to cristae remodeling and plays key roles in maintaining systemic energy balance by elevating energy expenditure and pedestrian locomotion. [ABSTRACT FROM AUTHOR]

General Control Non-repressed 5 protein (GCN5), encoded by the mammalian gene Kat2a , is the first histone acetyltransferase discovered to link histone acetylation to transcriptional activation [1]. The enzymatic activity of GCN5 is linked to cellular metabolic and energetic states regulating gene expression programs. GCN5 has a major impact on energy metabolism by i) sensing acetyl-CoA, a central metabolite and substrate of the GCN5 catalytic reaction, and ii) acetylating proteins such as PGC-1α, a transcriptional coactivator that controls genes linked to energy metabolism and mitochondrial biogenesis. PGC-1α is biochemically associated with the GCN5 protein complex during active metabolic reprogramming. In the first part of the review, we examine how metabolism can change GCN5-dependent histone acetylation to regulate gene expression to adapt cells. In the second part, we summarize the GCN5 function as a nutrient sensor, focusing on non-histone protein acetylation, mainly the metabolic role of PGC-1α acetylation across different tissues. • GCN5 regulates gene expression programs involved in metabolism. • GCN5 activity is sensitive to Acetyl-CoA levels, a central metabolite in the cell. • GCN5 acetylates PGC-1α to regulate its function as a transcriptional activator. • PGC-1α regulates liver glucose homeostasis and thermogenesis in adipose tissue. [ABSTRACT FROM AUTHOR]