Ghrelin and the Control of Energy Balance in Females

Abstract

Ghrelin is considered one of the most potent orexigenic peptide hormones and one that promotes homeostatic and hedonic food intake. Research on ghrelin, however, has been conducted predominantly in males and particularly in male rodents. In female mammals the control of energy metabolism is complex and it involves the interaction between ovarian hormones like estrogen and progesterone, and metabolic hormones. In females, the role that ghrelin plays in promoting feeding and how this is impacted by ovarian hormones is not well understood. Basal ghrelin levels are higher in females than in males, and ghrelin sensitivity changes across the estrus cycle. Yet, responses to ghrelin are lower in female and seem dependent on circulating levels of ovarian hormones. In this review we discuss the role that ghrelin plays in regulating homeostatic and hedonic food intake in females, and how the effects of ghrelin interact with those of ovarian hormones to regulate feeding and energy balance.

Approach of Acromegaly during Pregnancy

“…Pituitary GH does not cross the placenta; thus, there are no negative effects on the fetus even in acromegalic patients. In females with intact GH function, IGF1 physiologically decreases during the first trimester of pregnancy, while GH remains stable [ 33 , 34 , 35 ].…”

“…Then, the placental GH (also, known as GH2) takes control of pituitary GH under the physiological circumstances of a non-acromegalic gestation [ 33 , 34 ]. Placental GH secretion is continuous, not pulsatile; it is first detected at week 5, and by week 15 it progressively becomes the main circulating form of GH, which stimulates liver production of IGF1 and inhibits pituitary GH in non-acromegalic females [ 33 , 34 , 35 ]. GH2 remains the main player until week 37 [ 33 , 34 ].…”

“…Placental GH secretion is continuous, not pulsatile; it is first detected at week 5, and by week 15 it progressively becomes the main circulating form of GH, which stimulates liver production of IGF1 and inhibits pituitary GH in non-acromegalic females [ 33 , 34 , 35 ]. GH2 remains the main player until week 37 [ 33 , 34 ]. The shift from one type of GH to another might explain the small reduction of IGF1 levels amid the first pregnancy trimester [ 33 , 34 , 35 , 36 , 37 ].…”

“…GH2 remains the main player until week 37 [ 33 , 34 ]. The shift from one type of GH to another might explain the small reduction of IGF1 levels amid the first pregnancy trimester [ 33 , 34 , 35 , 36 , 37 ].…”

“…Physiologically, IGF1 will later increase due to placental GH stimulation (a peak during week 37); it provides essential growth-promoting effects on both the placenta and the fetus (among others, IGF1 represents the major regulator of development concerning most organs, including the central nervous system where it controls glucose metabolism) [ 33 , 34 , 35 , 36 , 37 ]. In acromegaly, IGF1 usually remains stable throughout the remaining period of gestation time because of the estrogen-induced state of GH resistance that prevents somatotropinoma-associated production of pituitary GH to have clinical and metabolic fetal consequences [ 36 , 38 ].…”