Obesity and insulin resistance (IR) in later life have been associated to nutritional insults in early life (Chooi et al., 2019; Facchi et al., 2020; Hasebe et al., 2021; Ribeiro et al., 2021). Adversities in the maternal environment during the babies’ development have a direct relationship with the way how the regulation of metabolism occurs in adulthood, which makes the suckling period an important neuroendocrine plasticity stage and makes the components in the milk a pivotal source of nutrition for babies (Palou et al., 2018; Pico et al., 2020).

Changes in milk nutrients and hormone composition put out offspring into a metabolic unhealthy status by programming impairment in energy metabolism and glucose homeostasis (Badillo-Suarez et al., 2017). Overfeeding during early postnatal life has been shown to favor the later development of metabolic dysfunction, which is associated with neuroendocrine hypothalamic circuitry derangement, during this critical plasticity window (Davidowa and Plagemann, 2004; Heidel et al., 1999; Plagemann et al., 1992). In addition, it programs overweight, IR and glucose intolerance in adulthood (de Almeida et al., 2013; Malta et al., 2016; Ribeiro et al., 2021; Rinaldi et al., 2014), corroborating the developmental origins of health and disease (DOHaD) concept.

Stressful insults in early life such as parental perturbations including undernutrition, rich-calorie diet consumption, exposure to endocrine disruptors, among several other physiological stress can imprint offspring's risk to develops some chronic diseases in adulthood implicates DOHaD concept (Barker, 2007; Gluckman et al., 2005). In this regard, the early overfeeding due to small litter is an interesting rat-model to study long-term metabolic consequence (DOHaD concept) associated to hypothalamic impairments (Plagemann et al., 2009).

In general, metabolic disruptions likewise IR, are linked to a chronic low-grade inflammation (Saltiel and Olefsky, 2017). The role of pro-inflammatory cytokine interleukin 6 (IL-6) (Bobbo et al., 2019), interleukin 1 beta (IL-1β) (Dror et al., 2017) and tumor necrosis factor alpha (TNF-α) (Hotamisligil et al., 1993) is known by exert metabolic effects, most notably being implicated in IR and obesity. The activation of the hypothalamic pro-inflammatory response has been shown in high-fat diet-induced obese rats (De Souza et al., 2005), as well early overfeed rats displayed white adipose tissue inflammation (Kayser et al., 2015), although mechanism underlying the obesity-induced inflammation and/or inflammation-induced IR, which can influence the onset of metabolic syndrome are not yet well understand.

To date, many efforts have been made in the quest to treat and/or prevent metabolic comorbidities. Among different of them, the use of bioactive molecules and functional foods as nutraceutical approach (Asgary et al., 2018; Cicero et al., 2018; Mathias et al., 2014) compound some of the evidences about benefits of the non-pharmacological interventions. In this field, using functional food such as calcium (Conceicao et al., 2017), fish oil (Dai et al., 2016) and soy isoflavones (Ribeiro et al., 2021) as nutraceutical intervention to prevent metabolic derangements in early overfeeding rats highlights the role of functional food on prevents long-term effects of early programming of IR. In addition, plant extracts’ compounds, such as phaseolamin, a present substance in white beans (Phaseolus vulgaris L.), have properties to control blood glucose levels. On this field, the role of white beans and its derived on weight loss and glycemic control have been reported (Barrett and Udani, 2011; Shi et al., 2020), although few is known about the mechanisms by which white beans can ameliorate these metabolic features.

In the current study, our aim was to test the hypothesis that the obese phenotype and metabolic dysfunctions featured in the post-natal overfeeding rats is associated with central inflammatory cytokines, and that it can be prevented by the consumption of white beans-supplemented diet.