Pinto bean supplementation improves maternal metabolic outcomes in a high-fat diet-induced obesity model of pregnancy

BACKGROUND: Maternal obesity is linked to dysregulated lipid metabolism, inflammation, and altered gut microbiota, which together can compromise placental function and fetal development. Pinto beans (PB), a fiber and polyphenol rich legume, may mitigate metabolic dysfunction during pregnancy. METHODS: Female C57BL/6 mice (n=20/group) were fed a control diet (CON) or high fat diet (HFD) for six weeks, randomized (n=10/group) to continue with or without 10% PB for an additional six weeks before and during pregnancy. Dams were euthanized at gestational day (GD) 17-17.5 and maternal and fetal tissues were collected. Body composition, serum lipids, maternal hepatic gene and protein expression, gut microbiota composition, placental morphology, and fetal hepatic and placental gene expression were assessed. Generalized linear and mixed models (dams as the experimental unit) approach was used for analyses. RESULTS: HFD increased % fat mass (26% vs 19%) and decreased %lean mass (74% vs 81%; both p < 0.05). In HFD-fed dams, PB lowered total cholesterol (43.4 vs 69.5 mg/dL), non-HDL cholesterol (10.3 vs 16.3 mg/dL), and triglycerides (48.1 vs 68.7 mg/dL; all p<0.05). PB reduced hepatic gene expression of Srebp1c ∼35% (p=0.047), Hmgcr expression by ∼36% (p=0.015), and reduced hepatic malonyl-CoA-acyl carrier transacylase abundance ∼23-27% (p<0.001). HFD+PB had higher gut microbial richness (Chao1) than HFD (p=0.036),. Litter size tended to be higher with PB (CON+PB: 9.2 vs HFD:7.4, p=0.07, HFD+PB:9.3 vs HFD:7.4, p=0.056). Placental weight was ∼35% lower in female HFD+PB than CON+PB (p=0.014). PB increased Placental Fatp1 ∼10-fold in CON fed mice (p<0.05), and placental necrosis varied by sex (decidual HFD vs CON males, p=0.01; junctional zone, HFD+PB vs CON+PB females, p=0.03). CONCLUSION: PB supplementation reduced serum cholesterol and triglycerides in HFD-fed dams, reduced hepatic lipogenic gene expression, and greater gut microbial richness. Placental and fetal differences were modest and sex- and diet-dependent, affecting placental necrosis.