Emulsifiers during gestation: The risks of ultra-processed food revealed in mice

Abstract

Several dietary components disrupt the control of energy balance. A new study in PLOS Biology shows that, in mice, maternal consumption of emulsifiers induces a rewiring of the hypothalamic feeding circuits and causes neuropsychological impairment in the offspring.

Fig 1. Alterations of the hypothalamic circuitry controlling energy balance after maternal exposure to compounds found in ultra-processed food.

Food additives such as emulsifiers, sweeteners, and EDCs affect circuits in the hypothalamus that control energy balance in the offspring of mice exposed during pregnancy. Male offspring exposed to emulsifiers during gestation and lactation displayed moderate glucose intolerance associated with a delayed postnatal leptin surge and a higher density of α-MSH staining in the PVN [5]. Gestational exposure to sweeteners led to increased adiposity and glucose intolerance and reorganized hypothalamic melanocortin circuits in male, but not female, offspring [4]. Young male and female mice perinatally exposed to low-dose EDCs showed a delayed postnatal leptin surge during postnatal development as well as reduced density of POMC projections into the PVN. The same exposure induced glucose intolerance in adult male and hyperphagic and obesity-prone phenotype in females exposed to high-fat diet [9]. Early postnatal exposure to the phytoestrogen genistein from postnatal day 1 to 8 significantly decreased POMC immunoreactivity in females, but not in males. Those females presented an increase in body weight and altered plasma concentrations of metabolic hormones [10]. Red highlights indicate potential sites of action of food additives. Parts of the figure were drawn by using pictures from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License. 3V, third ventricle; ARC, arcuate nucleus; EDCs, endocrine-disrupting chemicals; PVN, paraventricular network; VMH, ventromedial hypothalamus.