Despite the important role of inflammation-related factors on the occurrence of chronic diseases, there is still conflicting evidence about the effects of the ketogenic diet (KD) on these factors. In order to obtain a better viewpoint, this study aimed to comprehensively investigate the effects of a KD on inflammation-related markers. To find pertinent randomized controlled trials up to August 2023, databases including PubMed/Medline, Web of Science, Scopus, Cochrane Library, and Embase were searched. This study included all randomized controlled trials investigating the effects of a KD on C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-8, and IL-10 levels. Pooled weighted mean difference (WMD) and 95% confidence intervals (CIs) were achieved by random-effects model analysis for the best estimation of outcomes. Forty-four studies were included in this article. The pooled findings showed that a KD has an effect on lowering TNF-α (WMD: −0.32 pg/mL; 95% CI: −0.55, −0.09; P = 0.007) and IL-6 (WMD: −0.27 pg/mL; 95% CI: −0.52, −0.02; P = 0.036) compared with control groups. However, no significant effect was reported for others inflammation marker–related levels. The results of the subgroup analysis showed that, in trials following the KD for ≤8 weeks and in people aged ≤50 years, the reduction in TNF-α levels was significantly higher than in other groups. In addition, in people with a body mass index greater than 30 kg/m² compared to a body mass index ≤30 kg/m², IL-6 levels decreased to a greater extent after receiving the KD. Consequently, adherence to a KD appears to improve some markers associated with inflammation, including TNF-α and IL-6.

Obesity, which is the accumulation of fat in adipose tissue, has adverse impacts on human health. Obesity-related metabolic dysregulation has similarities to the metabolic alterations observed in aging. It has been shown that the adipocytes of obese individuals undergo cellular aging, known as senescence. Senescence can be transmitted to other normal cells through a series of chemical factors referred to as the senescence-associated secretory phenotype (SASP). Most of these factors are pro-inflammatory compounds. The immune system removes these senescent T-cells, but immunosenescence, which is the senescence of immune cells, disrupts the clearance of senescent T-cells. Immunosenescence occurs as a result of aging or indirectly through transmission from senescent tissues. The significant occurrence of senescence in obesity is expected to cause immunosenescence and impairs the immune response to resolve inflammation. The sustained and chronic inflammation disrupts insulin's metabolic actions in metabolic tissues. Therefore, this review focuses on the role of senescent adipocyte cells in obesity-associated immunosenescence and subsequent metabolic dysregulation. Moreover, the article suggests novel therapeutic approaches to improve metabolic syndrome by targeting senescent T-cells or using senotherapeutics. Graphical Abstract

The relationships between the total antioxidant capacity (TAC) of the diet and the risk of non-alcoholic fatty liver disease (NAFLD) have not previously been assessed. The aim of this study was to assess relationships between DTAC and odds of NAFLD in a case–control study. This case–control study was carried out in 158 patients with NAFLD and 357 healthy individuals aged 18–55 years. Dietary data were collected using validated 168-item quantitative food frequency questionnaires. Triacylglycerols (TAGs), total cholesterol (TC), high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C) and fasting blood glucose (FBS) concentrations were assessed using enzymatic methods and commercial kits. The DTAC was calculated based on the oxygen radical absorbance capacity of each food reported by the U.S. Department of Agriculture. The mean ± sd (standard deviation) for age and body mass index (BMI) of the study participants were 43⋅9 years ±5⋅9 and had 30⋅5 kg/m² ±2⋅6. The NAFLD patients included higher BMI and female proportion, compared with the control group. The NAFLD patients included higher smoking rates, biochemical parameters (TG, TC, LDL-C and FBS) and DTAC scores, compared with control groups (P-value < 0⋅05). However, patients with NAFLD had lower HDL levels and physical activities, compared with the control group. The highest tertile of DTAC showed lower odds of NAFLD, compared with the lowest tertile. This association was significant after adjustment for potential confounders (OR, 0⋅19; 95 % CI, 0⋅9–0⋅34; P for trend 0⋅001). Findings suggest that the promotion of naturally increased antioxidant capacities may help prevent odds of NAFLD.

Context: Some evidence has shown an association between maternal vitamin B12 levels and the development of preeclampsia in pregnant women, but the relationship between preeclampsia and vitamin B12 is not clear. Objective: The aim of this systematic review was to compare serum vitamin B12 levels in women with preeclampsia with those in normotensive pregnant women. Data Sources: The PubMed/MEDLINE, Scopus, and Web of Science databases were searched up to August 2019, along with the reference lists of included articles. Study Selection: The literature was searched for observational studies that investigated vitamin B12 levels in women with preeclampsia. Data Extraction: Data were extracted independently by 2 authors. Data were pooled using a random-effects model. Results: Vitamin B12 levels in women with preeclampsia were significantly lower than those in healthy women (mean, −15.24 pg/mL; 95%CI, −27.52 to −2.954; P < 0.015), but heterogeneity between studies was high (I2 = 97.8%; P = 0.0103). Subgroup analyses based on folic acid supplementation, homocysteine concentrations, and gestational age at the time of sampling for vitamin B12 assessment did not identify the sources of heterogeneity. Conclusions: Women with preeclampsia had significantly lower vitamin B12 concentrations than normotensive pregnant women.

Background: The aim of this study was to evaluate the serum level of matrix metalloproteinase 7 (MMP7) in infants with cholestasis and the diagnostic values of this biomarker to differentiate biliary atresia (BA) from other causes of cholestasis. Methods: This multi-center study is conducted during 2 years in Mofid children’s hospital and Children’s Medical Center, Pediatrics Center of Excellence Tehran, Iran. 54 infants with cholestasis were enrolled in this study with a control group consists of 41 healthy infants with the same age. Serum samples were taken from all these patients to assess serum levels of MMP7, Gamma-glutamyl Transferase (GGT). For each biomarker, we calculated the sensitivity and specificity and other statistical characteristics. Results: There were 89 subjects, 22 patients with BA, 32 patients with non-BA cholestasis and 41 subjects as control group. The mean serum MMP7 levels in BA, non-BA cholestasis and control group was 15.91 ng/ml ± 6.64, 4.73 ng/ml ± 2.59 and 0.49 ng/ml ± 0.33, respectively. The best cut-off point is calculated 7.8 ng/ml for MMP7 and 434.5 U/L for GGT. The area under curve (AUC) for these two markers are 0.988 ± 0.008 and 0.854 ± 0.052, respectively. The sensitivity and specificity of MMP7 to differentiate biliary atresia from nonbiliary atresia cholestasis in our study was 95.5% and 94.5%, respectively. The sensitivity and specificity of GGT was 77.3% and 77.8%, respectively. These results show that the MMP7 has more sensitivity and specificity in differentiation. Conclusion: MMP7 demonstrated good accuracy to differentiate biliary atresia from other causes of cholestasis.