4.6 Article

Pregnancy-related plasticity of gastric vagal afferent signals in mice

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00357.2020

Keywords

food intake; gastric vagal afferents; growth hormone; pregnancy; satiety signals

Funding

  1. Robinson Research Institute, University of Adelaide
  2. Australian Government Research Training Program (RTP) Stipend Scholarship

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This study shows that gastric vagal afferent signaling is attenuated during pregnancy and is inversely associated with meal size. Growth hormone reduces the mechanosensitivity of gastric vagal afferents, suggesting that increased maternal growth hormone levels may play a role in mediating adaptations in gastric vagal afferent signaling during pregnancy. These findings have significant implications for the peripheral control of food intake during pregnancy.
Gastric vagal afferents (GVAs) sense food-related mechanical stimuli and signal to the central nervous system, to integrate control of meal termination. Pregnancy is characterized by increased maternal food intake, which is essential for normal fetal growth and to maximize progeny survival and health. However, it is unknown whether GVA function is altered during pregnancy to promote food intake. This study aimed to determine the mechanosensitivity of GVAs and food intake during early, mid-, and late stages of pregnancy in mice. Pregnant mice consumed more food compared with nonpregnant mice, notably in the light phase during midand late pregnancy. The increased food intake was predominantly due to light-phase increases in meal size across all stages of pregnancy. The sensitivity of GVA tension receptors to gastric distension was significantly attenuated in midand late pregnancy, whereas the sensitivity of GVA mucosal receptors to mucosal stroking was unchanged during pregnancy. To determine whether pregnancy-associated hormonal changes drive these adaptations, the effects of estradiol, progesterone, prolactin, and growth hormone on GVA tension receptor mechanosensitivity were determined in nonpregnant female mice. The sensitivity of GVA tension receptors to gastric distension was augmented by estradiol, attenuated by growth hormone, and unaffected by progesterone or prolactin. Together, the data indicate that the sensitivity of GVA tension receptors to tension is reduced during pregnancy, which may attenuate the perception of gastric fullness and explain increased food intake. Further, these adaptations may be driven by increases in maternal circulating growth hormone levels during pregnancy. NEW & NOTEWORTHY This study provides first evidence that gastric vagal afferent signaling is attenuated during pregnancy and inversely associated with meal size. Growth hormone attenuated mechanosensitivity of gastric vagal afferents, adding support that increases in maternal growth hormone may mediate adaptations in gastric vagal afferent signaling during pregnancy. These findings have important implications for the peripheral control of food intake during pregnancy.

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