Gomes · The Journal of nutritional biochemistry 2018 · controlled animal study · n=?

Maternal diet-induced obesity during suckling period programs offspring obese phenotype and hypothalamic leptin/insulin resistance.

Cited 68 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Animal research (controlled rodent model) with no human data.

PubMed 30179726 · doi:10.1016/j.jnutbio.2018.07.006 · record verified 2026-08-27

What was done

Female Wistar rats at delivery were randomly assigned to a standard rodent chow diet (control) or a diet-induced obesity regimen (chow, sweetened condensed milk, sucrose, and water) throughout the suckling period. All offspring were fed standard chow from weaning until 91 days of age. Investigators assessed maternal body fat, insulin resistance, and milk composition, as well as adult offspring adiposity, food intake, glucose metabolism, pancreatic histology, and hypothalamic leptin and insulin signaling proteins.

What was found

The abstract reports no numerical values, effect sizes, or confidence intervals. Mothers on the obesity-inducing diet exhibited increased body fat, insulin resistance, and altered milk composition. At 91 days of age, their offspring showed overweight, hyperphagia, increased adiposity, hyperinsulinemia, insulin resistance, pancreatic islet hypertrophy, and increased beta-cell proliferation. Hypothalamic analysis in these offspring revealed decreased levels of ObRb, JAK2, STAT-3, IRbeta, PI3K, Akt, and POMC, along with increased NPY.

Why it matters

The findings demonstrate that maternal nutritional excess limited exclusively to the lactation window can permanently disrupt central appetite regulation and peripheral metabolic health in adult offspring. This points to hypothalamic leptin and insulin signaling pathways as specific targets of developmental programming.

Limits

The study was conducted in Wistar rats, and findings cannot be directly assumed for human infants. The abstract omits sample sizes, numerical measurements, and variance data. The experiment did not test post-weaning dietary challenges or reversibility of the observed signaling deficits.

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