Regulation of testicular steroidogenesis

2) Irreversible adaptation to sperm competition . It has been suggested that the ancestor of the boreoeutherian mammals was a small mammal that required very large testes (perhaps rather like those of a hamster ) for sperm competition and thus had to place its testes outside the body. [44] This led to enzymes involved in spermatogenesis, spermatogenic DNA polymerase beta and recombinase activities evolving a unique temperature optimum, slightly less than core body temperature. When the boreoeutherian mammals then diversified into forms that were larger and/or did not require intense sperm competition they still produced enzymes that operated best at cooler temperatures and had to keep their testes outside the body. This position is made less parsimonious by the fact that the kangaroo , a non-boreoeutherian mammal, has external testicles. The ancestors of kangaroos might, separately from boreotherian mammals, have also been subject to heavy sperm competition and thus developed external testes, however, kangaroo external testes are suggestive of a possible adaptive function for external testes in large animals.

Recently, a specific peptide inhibitor for ATGL was isolated from white blood cells, specifically mononuclear cells. This peptide was originally identifed as being involved in the regulation of the G 0 to G 1 transition of the cell cycle . This peptide was, therefore, called G0G1 switch protein 2 (G0S2). The protein is found in numerous tissues, with highest concentrations in adipose tissue and liver. In adipose tissue G0S2 expression is very low during fasting but increases after feeding. Conversely, fasting or PPARα-agonists increase hepatic G0S2 expression. The protein has been shown to localize to LDs, cytoplasm, ER, and mitochondria. These different subcellular localizations likely relate to multiple functions for G0S2 in regulating lipolysis, the cell cycle , and, possibly, apoptosis via its ability to interact with the mitochondrial antiapoptotic factor Bcl-2. With respect to ATGL regulation, the binding of the enzyme to LDs and subsequent is dependent on a physical interaction between the N-terminal region of G0S2 and the patatin domain of ATGL.

The venous system is somewhat unique because the spermatic veins are thin-walled, poorly muscularized, and lack effective valves except at the inflow points into the inferior vena cava or the renal vein. The right spermatic vein usually drains into the vena cava. The left spermatic vein drains into the left renal vein. The renal vein on the left side is thought to have a higher intraluminal pressure because the vein is compressed as it passes between the superior mesenteric artery and the aorta. This "nutcracker effect" may impair flow through the left renal and spermatic veins, especially in young men with limited retroperitoneal fat. The differential anatomy of the left and right spermatic veins is thought to explain, at least in part, the higher prevalence of varicoceles on the left side. The exact mechanism by which varicoceles cause infertility is unknown. In animal models, varicoceles are associated with increased blood flow to the testis and increased interstitial fluid in the testis. These two findings may impair regulation of testicular temperature and decrease intratesticular concentrations of testosterone or other local factors important for spermatogenesis.

Regulation of testicular steroidogenesis

regulation of testicular steroidogenesis

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