Non-pharmacological early weaning (NPEW) induces liver damage in male progeny at adulthood; however, pharmacological early weaning (PEW) does not cause this dysfunction. To elucidate this difference in liver dysfunction between these two models and determine the phenotype of female offspring, de novo lipogenesis, β-oxidation, very low-density lipoprotein (VLDL) export, and gluconeogenesis in both sexes were investigated in the adult Wistar rats that were weaned after a normal period of lactation (control group) or early weaned either by restriction of access to the dams’ teats (NPEW group) or by reduction of dams’ milk production with bromocriptine (PEW group). The offspring received standard diet from weaning to euthanasia (PN180). NPEW males had higher plasma triglycerides and TyG index, liver triglycerides, and cholesterol by de novo lipogenesis, which leads to intracellular lipids accumulation. As expected, hepatic morphology was preserved in PEW males, but they showed increased liver triglycerides. The only molecular difference between PEW and NPEW males was in acetyl-CoA carboxylase-1 (ACC-1) and stearoyl-CoA desaturase-1 (SCD-1), which were lower in PEW animals. Both early weaning (EW) females had no changes in liver cholesterol and triglyceride contents, and the hepatic cytoarchitecture was preserved. The expression of microsomal triglyceride transfer protein was increased in both the female EW groups, which could constitute a protective factor. The changes in hepatic lipid metabolism in EW offspring were less marked in females. EW impacted in the hepatic cytoarchitecture only in NPEW males, which showed higher ACC-1 and SCD-1 when compared to the PEW group. As these enzymes are lipogenic, it could explain a worsened liver function in NPEW males.

The cognitive effects of bromocriptine (10 mg/day) in chronic neuroleptic-treated schizophrenic patients were studied in a 4-month trial. Ten neuropsychological variables were used for the evaluations. Nine patients and seven controls completed the study. They were tested three times: before the beginning of the study, and after 2 and 4 months of treatment. The results showed that treated patients globally performed significantly better than the controls (P < 0.05), and that the digit symbol substitution test was significantly improved (P < 0.03). The WAIS performance score was also significantly improved (P < 0.02). The picture arrangement test was improved, but did not reach significance (P < 0.07). Verbal tests were not improved. It therefore appears that addition of a D2 dopamine agonist in neuroleptic-treated patients can improve some of their cognitive functions. Two explanations can be proposed: i) bromocriptine decreases neuroleptic-induced motor side effects or ii) has an effect on a putative hypodopaminergic function in schizophrenia.