Revealing Edible Bird Nest as Novel Functional Foods in Combating Metabolic Syndrome: Comprehensive In Silico, In Vitro, and In Vivo Studies.

Metabolic dysfunction, which includes intra-abdominal adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hypertension, manifests into metabolic syndrome and related diseases. Therefore, the discovery of new therapies in the fight against metabolic syndrome is very challenging. This study aims to reveal the existence of an edible bird nest (EBN) as a functional food candidate that may be a new alternative in fighting metabolic syndrome. The study included three approaches: in silico molecular docking simulation, in vitro, and in vivo in rats fed on cholesterol- and fat-enriched diets. Four terpenoids of Bakuchiol, Curculigosaponin A, Dehydrolindestrenolide, and 1-methyl-3-(1-methyl-ethyl)-benzene in EBN have been identified through LCMS/MS-QTOF. In molecular docking simulations, Bakuchiol and Dehydrolindestrenolide are considered very potent because they have higher inhibitory power on the four receptors (iNOS, ROS1 kinase, FTO, and lipase) than standard drugs. In vitro tests also provide insight into the antioxidant, antidiabetic, and antiobesity activities of EBN, which is quite feasible due to the smaller EC50 value of EBN compared to standard drugs. Interestingly, in vivo studies also showed significant improvements (p < 0.05) in the lipid profile, blood glucose, enzymatic levels, and inflammatory biomarkers in rats given high-dose dietary supplementation of EBN. More interestingly, high-dose dietary supplementation of EBN upregulates PGC-1α and downregulates HMG-CoA reductase. Comprehensively, it has been revealed that EBN can be novel functional foods for combating metabolic syndrome.

Dietary Supplementation of Caulerpa racemosa Ameliorates Cardiometabolic Syndrome via Regulation of PRMT-1/DDAH/ADMA Pathway and Gut Microbiome in Mice.

This study evaluated the effects of an aqueous extract of Caulerpa racemosa (AEC) on cardiometabolic syndrome markers, and the modulation of the gut microbiome in mice administered a cholesterol- and fat-enriched diet (CFED). Four groups of mice received different treatments: normal diet, CFED, and CFED added with AEC extract at 65 and 130 mg/kg body weight (BW). The effective concentration (EC50) values of AEC for 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), and lipase inhibition were lower than those of the controls in vitro. In the mice model, the administration of high-dose AEC showed improved lipid and blood glucose profiles and a reduction in endothelial dysfunction markers (PRMT-1 and ADMA). Furthermore, a correlation between specific gut microbiomes and biomarkers associated with cardiometabolic diseases was also observed. In vitro studies highlighted the antioxidant properties of AEC, while in vivo data demonstrated that AEC plays a role in the management of cardiometabolic syndrome via regulation of oxidative stress, inflammation, endothelial function (PRMT-1/DDAH/ADMA pathway), and gut microbiota.

Medical nutrition therapy in hemodynamically unstable patients due to cardiogenic shock with infected bronchiectasis and severe protein-energy malnutrition.

OBJECTIVE: Cardiogenic shock is defined as tissue hypoperfusion due to cardiac dysfunction. It is associated with hemodynamic unstability and elevated arterial lactate as one indicator for anaerobic metabolism. Hypercatabolic state in this condition leads to increasing nutritional requirement and negative nitrogen balance. Therefore, medical nutrition therapy by considering metabolic tolerance can prevent further metabolic deterioration and loss of lean mass and improve the patient's clinical outcome. METHODS: A 44-years-old female patient with severe protein-energy malnutrition (Subjective Global Assessment Score C; MUAC 15cm) suffered from hemodynamic unstability due to cardiogenic shock and infected bronchiectasis at the infection center of Wahidin Sudirohusodo Hospital. Intake was postponed due to mean arterial pressure 56mmHg on vasopressor support and oxygen saturation below 93%. Physical examinations showed loss of subcutaneous fat, lung crackles and wheezing, muscle wasting, and pretibial edema. Laboratory assessments showed elevated arterial lactate (3.2mmol/L), hypoalbuminemia (2.4g/dL), lymphocytopenia (650/µL), elevated liver enzymes (SGOT 780U/L; SGPT 868U/L), and urine urea nitrogen (5g/24h). Nutritional therapy was started after mean arterial pressure ≥65mmHg with a stable dosage of the vasopressor drug and decreased arterial lactate level to 2.2mmol/L then given gradually with a target calorie of 1500kcal and protein 1.5-1.8g/kg ideal body weight/day using high protein diet. Arterial lactate and blood gass analyses were controlled every day to determine the target of nutritional therapy day by the day. Snakehead fish extract, zinc, vitamin B complex, Thiamine, vitamin C, vitamin A, vitamin D3, and Curcumin were supplied. RESULT: After 15 days of nutritional therapy, the patient was discharged from the hospital with stable hemodynamic without vasopressor support, adequate nutritional intake, improvement of anthropometric parameters, and laboratory test results (arterial lactate 1.6mmol/L, albumin 3.1g/dL, lymphocyte 1.871/µL, SGOT 34U/L, SGPT 41U/L, urine urea nitrogen 0.72g/24h). CONCLUSION: Adequate nutritional therapy, which is planned by evaluating hemodynamic tolerance, can improve patient clinical outcomes and positive nitrogen balance in the hemodynamically unstable patient.

Medical nutrition therapy in hemodynamically unstable patients due to cardiogenic shock with infected bronchiectasis and severe protein-energy malnutrition

Objective: Cardiogenic shock is defined as tissue hypoperfusion due to cardiac dysfunction. It is associated with hemodynamic unstability and elevated arterial lactate as one indicator for anaerobic metabolism. Hypercatabolic state in this condition leads to increasing nutritional requirement and negative nitrogen balance. Therefore, medical nutrition therapy by considering metabolic tolerance can prevent further metabolic deterioration and loss of lean mass and improve the patient's clinical outcome. Methods: A 44-years-old female patient with severe protein-energy malnutrition (Subjective Global Assessment Score C; MUAC 15 cm) suffered from hemodynamic unstability due to cardiogenic shock and infected bronchiectasis at the infection center of Wahidin Sudirohusodo Hospital. Intake was postponed due to mean arterial pressure 56 mmHg on vasopressor support and oxygen saturation below 93%. Physical examinations showed loss of subcutaneous fat, lung crackles and wheezing, muscle wasting, and pretibial edema. Laboratory assessments showed elevated arterial lactate (3.2 mmol/L), hypoalbuminemia (2.4 g/dL), lymphocytopenia (650/μL), elevated liver enzymes (SGOT 780 U/L; SGPT 868 U/L), and urine urea nitrogen (5 g/24 h). Nutritional therapy was started after mean arterial pressure ≥65 mmHg with a stable dosage of the vasopressor drug and decreased arterial lactate level to 2.2 mmol/L then given gradually with a target calorie of 1500 kcal and protein 1.5–1.8 g/kg ideal body weight/day using high protein diet. Arterial lactate and blood gass analyses were controlled every day to determine the target of nutritional therapy day by the day. Snakehead fish extract, zinc, vitamin B complex, Thiamine, vitamin C, vitamin A, vitamin D3, and Curcumin were supplied. (AU)