We sought to examine the effects of daily consumption of macadamia nuts on body weight and composition, plasma lipids and glycaemic parameters in a free-living environment in overweight and obese adults at elevated cardiometabolic risk. Utilising a randomised cross-over design, thirty-five adults with abdominal obesity consumed their usual diet plus macadamia nuts (~15 % of daily calories) for 8 weeks (intervention) and their usual diet without nuts for 8 weeks (control), with a 2-week washout. Body composition was determined by bioelectrical impedance; dietary intake was assessed with 24-h dietary recalls. Consumption of macadamia nuts led to increased total fat and MUFA intake while SFA intake was unaltered. With mixed model regression analysis, no significant changes in mean weight, BMI, waist circumference, percent body fat or glycaemic parameters, and non-significant reductions in plasma total cholesterol of 2⋅1 % (-4⋅3 mg/dl; 95 % CI -14⋅8, 6⋅1) and low-density lipoprotein (LDL-C) of 4 % (-4⋅7 mg/dl; 95 % CI -14⋅3, 4⋅8) were observed. Cholesterol-lowering effects were modified by adiposity: greater lipid lowering occurred in those with overweight v. obesity, and in those with less than the median percent body fat. Daily consumption of macadamia nuts does not lead to gains in weight or body fat under free-living conditions in overweight or obese adults; non-significant cholesterol lowering occurred without altering saturated fat intake of similar magnitude to cholesterol lowering seen with other nuts. Clinical Trial Registry Number and Website: NCT03801837 https://clinicaltrials.gov/ct2/show/NCT03801837?term = macadamia + nut&draw = 2&rank = 1.

UNASSIGNED: Cardiovascular diseases (CVD) are leading cause of mortality in patients with type 2 diabetes mellitus (T2DM). Increased soluble sP-selectin and 715Thr > Pro polymorphism were studied in CVD and T2DM, but association between them hasn\'t been explored in Saudi Arabia. We aimed to assess sP-selectin levels in T2DM and T2DM-associated CVD patients in comparison to healthy control cohort. Also, we sought to investigate relationship between Thr715Pro polymorphism and sP-selectin levels and disease state.
UNASSIGNED: This is a cross-sectional case-control study. sP-selectin level (measured by Enzyme-linked immunosorbent assay) and prevalence of Thr715Pro polymorphism (assessed by Sanger sequencing) were investigated in 136 Saudi participants. The study comprised 3 groups: group1 included 41 T2DM patients; group 2 (48 T2DM patients with CVD), and group 3 (47 healthy controls).
UNASSIGNED: sP-selectin levels were significantly higher in diabetics and diabetics + CVD groups as compared to the corresponding control. In addition, results showed that the prevalence of 715Thr > Pro polymorphism is 11.75 % in the study population amongst the three study groups (9.55 % Thr/Pro, and 2.2 % Pro/Pro). No statistical difference was found between sP-selectin levels in subject carrying the wildtype genotype of this polymorphism and these who carry the mutant gene. There could be an association between this polymorphism and T2DM, whilst the polymorphism may protect diabetic patients from having CVD. However, odds ratio is not statistically significant in both cases.
UNASSIGNED: Our study supports the previous researches\' results that Thr715Pro is neither influencing the sP-selectin level nor the risk of CVD in T2DM patients.

Glycolipid metabolism disorder are major threats to human health and life. Genetic, environmental, psychological, cellular, and molecular factors contribute to their pathogenesis. Several studies demonstrated that neuroendocrine axis dysfunction, insulin resistance, oxidative stress, chronic inflammatory response, and gut microbiota dysbiosis are core pathological links associated with it. However, the underlying molecular mechanisms and therapeutic targets of glycolipid metabolism disorder remain to be elucidated. Progress in high-throughput technologies has helped clarify the pathophysiology of glycolipid metabolism disorder. In the present review, we explored the ways and means by which genomics, transcriptomics, proteomics, metabolomics, and gut microbiomics could help identify novel candidate biomarkers for the clinical management of glycolipid metabolism disorder. We also discuss the limitations and recommended future research directions of multi-omics studies on these diseases.

UNASSIGNED: Insulin resistance can be assessed by the Triglyceride-Glucose Index (TyG), a simple, low-cost, and easy-to-apply method.
UNASSIGNED: To assess the predictive capacity of the TyG index about cardiovascular risk and identify its cutoff point in a population at cardiometabolic risk.
UNASSIGNED: Cross-sectional study with 264 individuals at cardiometabolic risk (54.9% women, age: 43.1 ± 16.3 years). Demographic, anthropometric, clinical-laboratory, and lifestyle data were collected. The TyG index was determined using the formula Ln [fasting triglycerides (mg/dL) × fasting plasma glucose (mg (dL)/2]. The ten-year cardiovascular risk was assessed by the Framingham risk score (FRS). The receiver operating characteristic curve (ROC) was used to define the cutoff point for the TyG index, and the associations were tested by Poisson regression.
UNASSIGNED: ROC curve analysis indicated an area under the curve of 0.678 (95% CI = 0.618-0.734; p < 0.001), with a cutoff of 9.04 (sensitivity = 62.5%, specificity = 66.7%, positive predictive value = 29.4% and negative predictive value = 88.9%). Elevated TyG values ​​(≥9.04) were positively associated with cardiometabolic risk factors (total cholesterol, LDL, VLDL, uric acid, alanine aminotransferase, aspartate aminotransferase, waist-hip ratio, systolic blood pressure, HOMA-IR, smoking, metabolic syndrome, diabetes, and hepatic steatosis). After adjustment for confounding factors, individuals with high TyG showed an increase of 69% (RP = 1.69; 95%CI = 1.03-2.78) in the prevalence of intermediate/high risk by FRS, compared to those with low TyG.
UNASSIGNED: The TyG index showed a good predictive capacity for cardiovascular risk in ten years assessed by the FRS.

UNASSIGNED: Non-alcoholic fatty liver disease (NAFLD) is widespread chronic disease of the live in humans with the prevalence of 30% of the United States population.1,2 The goal of the study is to validate the performance of quantitative ultrasound algorithms in the assessment of hepatic steatosis in patients with suspected NAFLD.
UNASSIGNED: This prospective study enrolled a total of 31 patients with clinical suspicion of NAFLD to receive liver fat measurements by quantitative ultrasound and reference MRI measurements (proton density fat-fraction, PDFF). The following ultrasound (US) parameters based on both raw ultrasound RF (Radio Frequency) data and 2D B-mode images of the liver were analyzed with subsequent correlation with MRI-PDFF: hepatorenal index, acoustic attenuation coefficient, Nakagami coefficient parameter, shear wave viscosity, shear wave dispersion and shear wave elasticity. Ultrasound parameters were also correlated with the presence of hypertension and diabetes.
UNASSIGNED: The mean (± SD) age and body mass index of the patients were 49.03 (± 12.49) and 30.12 (± 6.15), respectively. Of the aforementioned ultrasound parameters, the hepatorenal index and acoustic attenuation coefficient showed a strong correlation with MRI-PDFF derivations of hepatic steatosis, with r-values of 0.829 and 0.765, respectively. None of the remaining US parameters showed strong correlations with PDFF. Significant differences in Nakagami parameters and acoustic attenuation coefficients were found in those patients with and without hypertension.
UNASSIGNED: Hepatorenal index and acoustic attenuation coefficient correlate well with MRI-PDFF-derived measurements of hepatic steatosis. Quantitative ultrasound is a promising tool for the diagnosis and assessment of patients with NAFLD.

Cardiometabolic disease (CMD), characterized with metabolic disorder triggered cardiovascular events, is a leading cause of death and disability. Metabolic disorders trigger chronic low-grade inflammation, and actually, a new concept of metaflammation has been proposed to define the state of metabolism connected with immunological adaptations. Amongst the continuously increased list of systemic metabolites in regulation of immune system, bile acids (BAs) represent a distinct class of metabolites implicated in the whole process of CMD development because of its multifaceted roles in shaping systemic immunometabolism. BAs can directly modulate the immune system by either boosting or inhibiting inflammatory responses via diverse mechanisms. Moreover, BAs are key determinants in maintaining the dynamic communication between the host and microbiota. Importantly, BAs via targeting Farnesoid X receptor (FXR) and diverse other nuclear receptors play key roles in regulating metabolic homeostasis of lipids, glucose, and amino acids. Moreover, BAs axis per se is susceptible to inflammatory and metabolic intervention, and thereby BAs axis may constitute a reciprocal regulatory loop in metaflammation. We thus propose that BAs axis represents a core coordinator in integrating systemic immunometabolism implicated in the process of CMD. We provide an updated summary and an intensive discussion about how BAs shape both the innate and adaptive immune system, and how BAs axis function as a core coordinator in integrating metabolic disorder to chronic inflammation in conditions of CMD.

UNASSIGNED: Cirrhosis of liver is associated with loss of liver function, portal hypertension, and pancreatic β-cell dysfunction leading to hepatogenous diabetes (HD). Often HD is an underestimated and understudied problem, particularly in the Indian subcontinent, where the prevalence of both Chronic liver disease (CLD) and diabetes is high. Hence this study was planned to highlight the prevalence of HD and its association with the severity of cirrhosis.
UNASSIGNED: A total of 121 cirrhotic patients without a history of diabetes were included in this prospective cross-sectional study. Seventy five g oral glucose tolerance test (OGTT) was done in all patients. Fasting serum insulin levels were done to calculate insulin resistance (IR) using homeostatic model assessment-insulin resistance (HOMA-IR). Upper gastrointestinal endoscopy was done to detect varices. Patients were divided into HD group and non-HD group for comparison of results.
UNASSIGNED: HD was seen in 52 (42.98%) patients; among them, 63.4% did not show evidence of HD by fasting plasma glucose (FPG) levels. Impaired glucose tolerance (IGT) was seen in 58 (47.93%) patients. Compared with the non-HD group, the HD group had significantly higher model for end-stage liver disease (MELD) score (P = 0.038), HOMA-IR (P < 0.001), incidence of large varices (P < 0.001) and variceal bleeding (P < 0.001). A statistically significant association was noted between HD and Hepatocellular carcinoma (HCC) (P < 0.001).
UNASSIGNED: Patients with cirrhosis had a high prevalence of IGT, IR, and HD. The presence of HD is well associated with the severity of cirrhosis in the form of higher MELD score (>15), CTP score (>10), higher bilirubin levels, large varices, bleeding varices, and HCC. FPG levels and glycated hemoglobin (HbA1c) cannot be relied upon, and OGTT aids in the unmasking of HD in these patients.

Gallstones are more common in patients with cirrhosis of the liver, and the incidence increases with severity of liver disease. Pigment stones are the most frequent type of gallstones (GSs) in cirrhotics, and majority remain asymptomatic. Hepatitis C virus infection and nonalcoholic fatty liver disease are the underlying etiologies of liver diseases that most often associated with GSs. Multiple altered mechanisms in cirrhosis such as chronic hemolysis due to hypersplenism, reduced bile acid synthesis and transport, decreased cholesterol secretion, decreased apolipoprotein A-I and A-II secretion, gallbladder hypo-motility, autonomic dysfunction, and portal hypertension collectively lead to increased risk of lithogenesis. Asymptomatic GSs should be followed up closely and offered laparoscopic cholecystectomy once symptomatic in Child-Pugh class A and B patients. The model for the end-stage liver disease score is the best predictor of the outcome after cholecystectomy. In patients of Child-Pugh class C, conservative or minimally invasive approaches should be used to treat complications of GSs.

OBJECTIVE: Apical periodontitis (AP) is a chronic or acute inflammatory disease usually developed from endodontic infections, predominantly due to gram-negative anaerobic bacteria invading the dental pulp. This study aimed to evaluate lymphocyte markers to assess the involvement of adaptive immunity in insulin resistance (IR) in a rat model of AP.Design.Forty-five male Wistar albino rats were divided into 3 groups (control, 1AP and 4AP). AP was induced in the upper right first molar (1AP), and in the first and second upper and lower right molars (4AP). The spleen was collected to evaluate the expression of transcription factors involved in lymphocyte polarization, including T-bet (Th1), GATA3 (Th2), and FOXP3 (Treg). Blood samples were assessed for serum cytokine levels transcribed by the respective lymphocyte polarizations, INF-γ (Th1), IL-4 (Th2) and TGF-β (Treg). In addition, glucose and insulin levels were measured to evaluate IR by the HOMA-IR method.
RESULTS: The results showed higher T-bet expression on AP groups, along with lower GATA3 and FOXP3 expression in the 1AP, in addition to increased GATA3 and decreased FOXP3 expression in the 4AP group compared to the CN group. There was no difference in the INF-γ levels, while IL-4 was decreased in the AP groups. Taken together, these results suggest that the adaptive immune system, with a predominance of the Th1 polarization, may be involved in the development of IR in rats with AP.
CONCLUSIONS: AP promotes increase in the expression of T-bet (4AP) and decrease of FOXP3 expressions and IL-4 levels (1AP and 4AP). However, depending on the number of lesions (1 or 4 lesions), the expression of GATA3 appears differently. Thus, innate immunity and adaptive immunity may contribute to the IR observed in rats with AP.

BACKGROUND: Noninvasive diagnostics of nonalcoholic fatty liver disease (NAFLD), the most common cause of liver dysfunction in children, are based on imaging, biochemical tests and their compilation. The study aimed to evaluate the serological biomarkers of steatosis, inflammation and liver fibrosis to assess the risk of NAFLD in children.
METHODS: A total of 73 children were included in the prospective study; 50 of them were diagnosed with NAFLD based on ultrasound, and 23 formed a control group. Basic anthropometric parameters were measured, blood samples were taken for laboratory tests and evaluated proteins were assessed by enzyme-linked immunosorbent assay-adiponectin, tumour necrosis factor alpha, fibroblast growth factor 21, liver fatty acid-binding protein (L-FABP) and interleukin 6.
RESULTS: Statistically significant differences between the levels of two proteins were found: the adiponectin level was lower in the NAFLD group (12.24 ± 7.01 vs 16.88 ± 9.21 μg/mL, P = 0.024), and L-FABP levels were higher (21.48 ± 20.61 vs 11.74 ± 8.39 ng/mL, P = 0.031). In the group of children with body mass index (BMI)-for-age >1 standard deviation (SD), adiponectin concentration was also significantly lower (12.18 ± 6.43 μg/mL) than in the group with BMI ≤1 SD (17.29 ± 9.42 μg/mL, P = 0.015). The odds ratios and 95% confidence interval for the relation between adiponectin and NAFLD and obesity were 0.868 (0.767-0.982) and 0.838 (0.719-0.977), respectively.
CONCLUSIONS: Adiponectin may be useful in evaluating the risk of NAFLD and obesity in children.