Myo-inositol (MI) supplementation mitigates metabolic dysregulation in lactating rats.

MI during lactation attenuated the pro-inflammatory state in liver and rWAT of dams.

Offspring of MI-supplemented dams showed improved glucose regulation at weaning.

MI during lactation confers metabolic benefits to both dams and their offspring.

Myo-inositol (MI) supplementation has emerged as a promising intervention to mitigate the malprogramming effects associated with adverse maternal conditions during the perinatal period. This study aimed to assess the effects of MI supplementation during lactation on metabolism in diet-induced obese rats and on early health outcomes in their offspring. Female Wistar rats were fed either a control (CON) or Western diet (WD) for one month before mating and during gestation and lactation. After parturition, dams were supplemented daily with either MI or vehicle (V) throughout lactation. Phenotypic traits, along with milk and blood parameters were analyzed in dams and their offspring during lactation. At weaning, hepatic lipid content and gene expression in the liver, retroperitoneal white adipose tissue (rWAT), and mammary gland were assessed in dams. MI supplementation significantly reduced hepatic lipid accumulation in WD-dams and decreased pro-inflammatory markers in the liver (Tnfa) and retroperitoneal white adipose tissue (rWAT) (Tnfa, Il6) in both CON- and WD-dams, as well as modulated milk insulin levels. Their offspring exhibited, in plasma, higher MI and BDNF concentrations as well as lower insulin levels, which are key factors in perinatal programming. These findings suggest that maternal MI supplementation during lactation confers metabolic benefits to both dams and their offspring, specifically improving maternal inflammation and lipid metabolism while influencing milk composition.

Maternal myo-inositol supplementation during lactation improves lipid metabolism, reduces inflammation and modulates mammary gland involution in dams, and promotes short-term glucose homeostasis in the offspring, suggesting that it could be a potential strategy to counteract the metabolic consequences of diet-induced obesity.

Myo-inositol

Lactation

Obesity

Inflammation

Perinatal programming

Lipid accumulation

Glucose homeostasis

brain-derived neurotrophic factor

carnitine palmitoyl transferase 1A

guanosine diphosphate dissociation Inhibitor

homeostasis model assessment of insulin resistance

non-alcoholic fatty liver disease

proliferating cell nuclear antigen

peroxisome proliferator-activated receptor alpha

prostaglandin-endoperoxide synthase 2

retroperitoneal white adipose tissue

sterol regulatory element-binding transcription factor 1

tumor necrosis factor alpha

© 2025 The Author(s). Published by Elsevier Inc.