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Hormonal physiology of lactation
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Rawan El-Amin, Loren Custer, Jennifer Silk
Lactogenesis involves the onset of milk production and secretion secondary to maturation of alveolar milk-producing cells.The first stage begins with the morphologic differentiation of mammary epithelial cells during mid-pregnancy to support production of colostrum.2 This stage is inhibited from further progression by high levels of progesterone during pregnancy.The transition to stage two occurs at parturition when the placenta is delivered and levels of progesterone, estrogen, and human placental lactogen (hPL) decrease while prolactin levels remain high, possibly corresponding to increased cortisol and insulin levels. As the inhibitory influence of progesterone is no longer present, α-lactalbumin production increases. This stimulates the enzyme lactose synthase to increase lactose and milk production.3 Thyroid hormones can also enhance the secretion of lactalbumin.Stage two of lactogenesis can be altered in patients with diabetes, elevated cortisol induced by stress during late stages of labor, cesarean delivery, and retained products of conception including delayed placenta extraction.1
Prolactin
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
The biochemical actions of PRL to initiate milk secretion in appropriately prepared mammary epithelial cells have been studied extensively. The hormone interacts initially with PRL receptors located in the plasma membrane of the cells of the mammary alveoli. The molecular structure of these PRL receptors was recently determined for rat liver tissue and the same receptors were also present in rat mammary tissue (Jahn et al., 1991). These authors also found that progesterone antagonized the usual periparturient increase in mammary receptors for PRL. This action may partly explain the observation that progesterone inhibits PRL-dependent lactogenesis in many species. As a result of PRL binding to its receptor in mammary cells, intracellular levels of mRNA encoding casein and a-lactalbumin proteins are increased. Both of these proteins are constituents of milk, but a-lactalbumin also comprises a part of the enzyme, lactose synthetase, that catalyzes the production of lactose for secretion into milk. As stated above, the liver has many PRL receptors but their functional role has not been fully determined. However, there is some evidence that PRL stimulates the liver to produce an unidentified factor which, together with PRL, acts on the mammary tissue to promote lactogenesis (English et al., 1990).
Reactivities of Amino Acids and Proteins with Iodine
Published in Erwin Regoeczi, Iodine-Labeled Plasma Proteins, 2019
Acylation of one tyrosine (and five amino groups) in goat a-lactalbumin results in 15% loss of lactose synthetase activating activity and 10% loss in galactose transferase activating activity.345 Slightly higher (approximately 25%) losses in lactose synthetase activating ac- tivity seem to occur when the enzyme is modified to the same extent by using tetranitro- methane or triiodide.346 α -Lactalbumin also tends to polymerize when treated with tetranitromethane.
Current and experimental drug therapy for the treatment of polycystic ovarian syndrome
Published in Expert Opinion on Investigational Drugs, 2020
Luigi Della Corte, Virginia Foreste, Fabio Barra, Claudio Gustavino, Franco Alessandri, Maria Grazia Centurioni, Simone Ferrero, Giuseppe Bifulco, Pierluigi Giampaolino
The treatment with Myo-inositol (MI) has shown good results for the improvement of insulin sensitivity in women affected by PCOS. In some clinical trials, MI was able to decrease glycemia after glucose tolerance test (OGTT) [67], homeostatic model assessment (HOMA) index, and secretion of LH, DHEA, testosterone, progesterone, and serum lipid profile [87]. Regarding its mechanism of action, MI prevents glucose absorption at the duodenal level and decreases glucose rise in blood acting on intestinal glucose uptake [88]. Furthermore, it improves insulin sensitivity in adipocytes by increasing lipid storage capacity and glucose uptake, and by inhibiting lipolysis. MI exerts its effects also via the expression of peroxisome proliferator-activated receptors gamma (PPAR-gamma) [89]. According to its safety profile, MI is a natural molecule, used as a nutritional supplement, which proved to be very safe. The US FDA included MI in the list of generally recognized as safe (GRAS) compounds [90]. MI, along with D-chiro-inositol (DCI), is the most important stereoisomers of inositol, molecules acting at different levels on glucose concentrations in the organism. Their physiological plasma ratio is 40:1, and a scientifically valid treatment should be based on this ratio [91]. In a study by Le Donne et al., a population of forty-three overweight/obese patients with PCOS were randomly treated for 6 months with only diet (group 1, n = 21), diet and MI (4 g) plus folic acid (400 µg) daily (group 2, n = 10); diet in association with MI (1.1) g plus D-chiroinositol (27.6 mg) plus folic acid (400 µg) daily (group 3, n = 13). The results showed that body weight, BMI, waist and hip circumferences decreased significantly in all groups; on the other hand, there was a significant difference between the three groups regarding the restoration of menstrual regularity (p = 0.02), which was obtained in all the patients of the group three [92]. It has also been suggested that a high concentration of MI in the ovarian microenvironment may improve the availability of follicles; moreover, when added to the diet, MI seems to accelerate the weight loss and to restore the regularity of the menstrual cycle, effectively increasing the chances of conception [92]. One-third of PCOS patients are resistant to inositol treatment: in these patients, inositol failed to improve the metabolic and hormonal parameters and restore ovulation significantly. The reason for this failure is not well established, but it has been hypothesized that such a problem can derive from the reduced or absent absorption of inositol due to unclear or unpredictable conditions (e.g. obesity, chronic intestinal diseases, dysbiosis) [67]. To increase the absorption, MI was combined with a ‘carrier’, the alpha-lactalbumin (alpha-LA) [93], a small milk protein component of lactose synthase, simple model Ca2+ binding protein. Alpha-LA can act not only as a carrier but also as a co-operator of MI, considering its role in improving glycemia [94] and reducing inflammatory status [95]. In detail, Alpha-LA can inhibit type 2 cyclooxygenase (COX 2) and decrease the production of inflammatory cytokines [95].