Abstract

Lactation is an important function that is dependent on changes in the maternal homeostasis and sustained by histological maternal adjustments. We evaluated how offspring manipulations during the lactational phase can modulate maternal morphologic aspects in the mammary gland, adipose tissue, and pancreatic islets of lactating dams. Two different models of litter-manipulation-during-lactation were used: litter sizes, small litters (SL) or normal litters (NL) and subcutaneous injections in the puppies of monosodium glutamate (MSG), or saline (CON). SL Dams and MSG Dams presented an increase in WAT content and higher plasma levels of glucose, triglycerides, and insulin, in relation to NL Dams and CON Dams, respectively. The MG of SL Dams and MSG Dams presented a high adipocyte content and reduced alveoli development and the milk of the SL Dams presented a higher calorie and triglyceride content, compared to that of the NL Dams. SL Dams presented a reduction in islet size and greater lipid droplet accumulation in BAT, in relation to NL Dams. SL Dams and MSG Dams present similar responses to offspring manipulation during lactation, resulting in changes in metabolic parameters. These alterations were associated with higher fat accumulation in BAT and changes in milk composition only in SL Dams.

Highlights

  • Lactation is a critical period in female life that requires a coordinate adaptation in energy metabolism

  • The area under curve (AUC) of food, water, and body weight gain were reduced by 37.4%, 36.2%, and 53.4%, respectively, in the small litters (SL) Dams, compared to the normal litters (NL) Dams (p < 0.05)

  • Hyperphagia is an evident characteristic of the lactation phase, an event attributed to changes in the central action of hypothalamic neuropeptides linked to the regulation of food intake [22,23,24]

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Summary

Introduction

Lactation is a critical period in female life that requires a coordinate adaptation in energy metabolism This period induces changes in morphologic aspects, in adipose and glandular tissues to sustain milk production [1, 2]. Obesogenic maternal diets, with an excess of nutrients, such as lipids or carbohydrates, can lead to changes in milk volume [3, 4] and milk composition, affecting lactose [5] and fat content [5, 6] In this regard, mice that are chronically exposed to a high fat diet present a reduction in mammary gland (MG) area, high leptin levels, and systemic prolactin resistance, which lead to impaired lactation performance [7]. Maternal obesity or undernutrition, during lactation, affects offspring growth, predisposing them to the development of obesity and cardiovascular disease in adult life [8, 9]

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