ABSTRACT
Carbohydrate intake restriction positively affects markers related to metabolic syndrome (MS). However, the effects of long-term carbohydrate-free diets (CFD) have yet to be studied. The main objective of this study was to report the effects on biochemical and morphometric parameters in a rat model of MS. Male Wistar rats were initially divided into two groups: the standard diet group (SD, n = 20); and the MS group (n = 30) fed a high-glucose diet. Ten animals from each group were sacrificed after 20 weeks on their respective diets to verify MS development. The remaining MS animals were divided into two subgroups: one continued with the MS diet (n = 10); and the other transitioned to a carbohydrate-free diet (MS + CFD group, n = 10) for 20 more weeks. At week 40, parameters, including glucose, insulin, lipid profile, ketone bodies, C-reactive protein (CRP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, creatinine, liver and muscle glycogen, and serum, hepatic, renal, and pancreatic malondialdehyde (MDA) levels were assessed. Transitioning to CFD resulted in decreased caloric intake and body weight, with normalized parameters including MDA, insulin, lipid profile, ALT, liver glycogen, creatinine, and CRP levels. This shift effectively reversed the MS-induced alterations, except for glycemia and uremia, likely influenced by the diet's high protein content stimulating gluconeogenesis. This research underscores the potential benefits of long-term carbohydrate restriction in mitigating MS-related markers.
ABSTRACT
BACKGROUND: Inadequate trophoblast invasion and the subsequent inflammatory response have been implicated in preeclampsia (PE) pathogenesis. Because MYC-induced nuclear antigen (MINA) gene expression is involved in cell proliferation and differentiation, inflammatory response modulation, and the unpaired regulation of which is associated with human diseases, we sought to investigate the connection between MINA and PE. OBJECTIVE: The aim of this study was to evaluate the possible relationship between the MINA rs4857304 variant and susceptibility to PE development as well as to estimate placental MINA gene expression and its association with PE. METHODS: About 242 pregnant women (126 PE cases and 116 controls) were included. MINA genotyping and gene expression were evaluated by quantitative real-time polymerase chain reaction using TaqMan probes. RESULTS: The G/G genotype of the MINA rs4857304 variant was associated with severe PE (p = 0.027, OR = 1.8, 95% CI = 1.8-3.2). Carriers of one G allele of the MINA rs4857304 variant exhibited a 1.7-fold increased risk of severe PE (p = 0.029, 95% CI = 1.1-3.0). MINA was underexpressed in preeclamptic placentas and MINA expression differed between the mild and severe PE groups. Differences in the expression levels of MINA were found among women with the T/T genotype of the rs4857304 polymorphism and carriers of at least one G allele (p = 0.024). CONCLUSION: PE and its severity are associated with the underexpression of placental MINA, and the G/G genotype of the MINA rs4857304 variant may modify the risk of severe PE among the PE cases evaluated.
