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Health & Wellness
Metformin therapy for restoration of female and male reproductive functions
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<blockquote data-quote="madman" data-source="post: 194163" data-attributes="member: 13851"><p><strong>Figure 2.</strong> <strong>The pathways involved in the inhibitory effect of metformin on hyperandrogenism in PCOS. Hyperinsulinemia and HA are among the key pathogenetic factors in the development of PCOS, which is why their attenuation by MF is the most important mechanism for improving the effectiveness of this drug on ovarian function in PCOS women. In PCOS, MF-induced increase in insulin sensitivity leads to a decrease in the HOMA-IR and a weakening of compensatory hyperinsulinemia. Another mechanism for lowering insulin levels may be an increase in the level of IGFBP-1, which specifically binds insulin and IGF-1. In PCOS, the expression of IGFBP-1 is generally reduced, and MF treatment may be one way to normalize it. Reduced hyperinsulinemia and an increase in IGFB-1 levels lead to a decrease in the stimulating effect of insulin and IGF-1 on ovarian steroidogenesis and a weakening of HA. Hyperinsulinemia leads to a decrease in the production of SHBG, which provokes HA in PCOS. MF-induced reduction of hyperinsulinemia leads to the normalization of the SHBG levels, thereby preventing excess androgen levels in the blood. By improving the functionality of the hypothalamic signaling network responsible for the pulsatile secretion of GnRH, treatment with MF leads to the normalization of blood LH levels and the LH/FSH ratio, both of which are increased in PCOS. A decrease in blood LH levels results in a weakening of gonadotropin-induced androgen production by the ovaries. A direct regulatory effect of MF on ovarian steroidogenesis was also established. By inhibiting the mitochondrial ETC complex I, stimulating the LKB1 activity and, as a result, increasing the AMPK activity, MF reduces the synthesis of androstenedione in the ovarian cells and prevents HA. It can be assumed that the prevalence of some mechanisms of the inhibitory effect of MF on HA is due to the characteristic features of PCOS pathogenesis and the metabolic and hormonal status of the ovaries. Details and bibliographic references are presented in Section 3.4. Abbreviations: AMPK, AMP-activated protein kinase; FSH, follicle-stimulating hormone; HA, hyperandrogenism; HOMA-IR, homeostasis model assessment of insulin resistance; IGF-1, insulin-like growth factor-1; IGFBP-1, insulin-like growth factor-binding protein-1; LH, luteinizing hormone; LKB1, liver kinase B1; SHBG, androgen, and sex hormone-binding globulin.</strong></p><p>[ATTACH=full]12500[/ATTACH]</p></blockquote><p></p>
[QUOTE="madman, post: 194163, member: 13851"] [B]Figure 2.[/B] [B]The pathways involved in the inhibitory effect of metformin on hyperandrogenism in PCOS. Hyperinsulinemia and HA are among the key pathogenetic factors in the development of PCOS, which is why their attenuation by MF is the most important mechanism for improving the effectiveness of this drug on ovarian function in PCOS women. In PCOS, MF-induced increase in insulin sensitivity leads to a decrease in the HOMA-IR and a weakening of compensatory hyperinsulinemia. Another mechanism for lowering insulin levels may be an increase in the level of IGFBP-1, which specifically binds insulin and IGF-1. In PCOS, the expression of IGFBP-1 is generally reduced, and MF treatment may be one way to normalize it. Reduced hyperinsulinemia and an increase in IGFB-1 levels lead to a decrease in the stimulating effect of insulin and IGF-1 on ovarian steroidogenesis and a weakening of HA. Hyperinsulinemia leads to a decrease in the production of SHBG, which provokes HA in PCOS. MF-induced reduction of hyperinsulinemia leads to the normalization of the SHBG levels, thereby preventing excess androgen levels in the blood. By improving the functionality of the hypothalamic signaling network responsible for the pulsatile secretion of GnRH, treatment with MF leads to the normalization of blood LH levels and the LH/FSH ratio, both of which are increased in PCOS. A decrease in blood LH levels results in a weakening of gonadotropin-induced androgen production by the ovaries. A direct regulatory effect of MF on ovarian steroidogenesis was also established. By inhibiting the mitochondrial ETC complex I, stimulating the LKB1 activity and, as a result, increasing the AMPK activity, MF reduces the synthesis of androstenedione in the ovarian cells and prevents HA. It can be assumed that the prevalence of some mechanisms of the inhibitory effect of MF on HA is due to the characteristic features of PCOS pathogenesis and the metabolic and hormonal status of the ovaries. Details and bibliographic references are presented in Section 3.4. Abbreviations: AMPK, AMP-activated protein kinase; FSH, follicle-stimulating hormone; HA, hyperandrogenism; HOMA-IR, homeostasis model assessment of insulin resistance; IGF-1, insulin-like growth factor-1; IGFBP-1, insulin-like growth factor-binding protein-1; LH, luteinizing hormone; LKB1, liver kinase B1; SHBG, androgen, and sex hormone-binding globulin.[/B] [ATTACH type="full"]12500[/ATTACH] [/QUOTE]
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Metformin therapy for restoration of female and male reproductive functions
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