Lactation as a programming window for metabolic syndrome

Abstract

The concept of developmental origins of health and disease (DOHaD) was initially supported by the low birth weight and higher risk of developing cardiovascular disease in adult life, caused by nutrition restriction during foetal development. However, other programming windows have been recognized in the last years, namely lactation, infancy, adolescence and even preconception. Although the concept has been developed in order to study the impact of foetal calorie restriction in adult life, it is now recognized that maternal overweight during programming windows is also harmful to the offspring. This article explores and summarizes the current knowledge about the impact of maternal obesity and obesogenic diets during lactation in the metabolic programming towards the development of metabolic syndrome in the adult life. The impact of maternal obesity and obesogenic diets in milk quality is discussed, including the alterations in specific micro and macronutrients, as well as the impact of such alterations in the development of metabolic syndrome-associated features in the newborn, such as insulin resistance and adiposity. Moreover, the impact of milk quality and formula feeding in infants' gut microbiota, immune system maturation and in the nutrient-sensing mechanisms, namely those related to gut hormones and leptin, are also discussed under the current knowledge.

Reverting to a Healthy Diet during Lactation Normalizes Maternal Milk Lipid Content of Diet‐Induced Obese Rats and Prevents Early Alterations in the Plasma Lipidome of the Offspring

“…[ 6–8 ] Although the specific mechanisms involved are only partially understood, [ 9 ] milk quality may represent one of the key factors. [ 10 ] Thus, intervention studies in rodents have shown that the intake of an obesogenic diet during the perinatal period negatively affects the structure and function of the mammary gland and therefore the composition of milk, [ 11 ] including altered metabolism‐regulating hormones and fatty acids (FA) profiles. [ 12,13 ]…”

Myo-Inositol Supplementation in Suckling Rats Protects against Adverse Programming Outcomes on Hypothalamic Structure Caused by Mild Gestational Calorie Restriction, Partially Comparable to Leptin Effects

“…Lactation represents a critical window of development, and adequate/optimal nutrition during this period may be overriding for the future metabolic health of the offspring, including the prevention of possible harmful programming effects due to adverse fetal conditions [ 41 ]. There is compelling evidence from intervention studies in animal models on the essential role of leptin ingested during lactation in the prevention of obesity and other related pathologies in adulthood since it ensures a correct programming and development of hypothalamic structures involved in energy metabolism [ 16 ].…”

Maternal Supplementation of Probiotics, Prebiotics or Postbiotics to Prevent Offspring Metabolic Syndrome: The Gap between Preclinical Results and Clinical Translation

“…The pathogenic interconnections between the gut microbiota and certain mechanisms are implicated in MetS of developmental origins. These core mechanisms include aberrant activation of the RAAS, oxidative stress, NO deficiency and dysregulated nutrient sensing signals [ 4 , 5 , 6 , 7 , 9 , 10 , 11 , 12 ].…”

“…Notably, different environmental insults in early life can program similar features of MetS, proposing a commonality of mechanistic pathways behind MetS of developmental origins. Despite these pathogenic mechanisms underlying developmental programming are still inconclusive, several common mechanisms have been reported, including nitric oxide (NO) deficiency, oxidative stress, aberrant activation of the renin-angiotensin-aldosterone system (RAAS), dysfunctional nutrient sensing signals, epigenetic regulation and gut microbiota dysbiosis [ 4 , 5 , 6 , 7 , 9 , 10 , 11 , 12 ].…”