Which gland produces testosterone

As growth proceeds, the column of cells may divide or give off offshoots, in which case a compound gland is formed. In many glands, the number of branches is limited, in others (salivary, pancreas) a very large structure is finally formed by repeated growth and sub-division. As a rule, the branches do not unite with one another, but in one instance, the liver, this does occur when a reticulated compound gland is produced. In compound glands the more typical or secretory epithelium is found forming the terminal portion of each branch, and the uniting portions form ducts and are lined with a less modified type of epithelial cell. [1]

The ONLY purpose of the parathyroid glands is to regulate the calcium level in our bodies within a very narrow range so that the nervous and muscular systems can function properly. This is all they do. They measure the amount of calcium in the blood every minute of every day... and if the calcium levels go down a little bit, the parathyroid glands recognize it and make parathyroid hormone (PTH) which goes to the bones and takes some calcium out (makes a withdrawal from the calcium vault) and puts it into the blood. When the calcium in the blood is high enough, then the parathyroids shut down and stop making PTH.

The levels of hormones in the body can be regulated by several factors. The nervous system can control hormone levels through the action of the hypothalamus and its releasing and inhibiting hormones. For example, TRH produced by the hypothalamus stimulates the anterior pituitary to produce TSH. Tropic hormones provide another level of control for the release of hormones. For example, TSH is a tropic hormone that stimulates the thyroid gland to produce T3 and T4. Nutrition can also control the levels of hormones in the body. For example, the thyroid hormones T3 and T4 require 3 or 4 iodine atoms, respectively, to be produced. In people lacking iodine in their diet, they will fail to produce sufficient levels of thyroid hormones to maintain a healthy metabolic rate. Finally, the number of receptors present in cells can be varied by cells in response to hormones. Cells that are exposed to high levels of hormones for extended periods of time can begin to reduce the number of receptors that they produce, leading to reduced hormonal control of the cell.

Lactiferous duct development occurs in females in response to circulating hormones . First development is frequently seen during pre- and postnatal stages, and later during puberty . Estrogen promotes branching differentiation, [34] whereas in males testosterone inhibits it. A mature duct tree reaching the limit of the fat pad of the mammary gland comes into being by bifurcation of duct terminal end buds (TEB), secondary branches sprouting from primary ducts [5] [35] and proper duct lumen formation. These processes are tightly modulated by components of mammary epithelial ECM interacting with systemic hormones and local secreting factors. However, for each mechanism the epithelial cells' " niche " can be delicately unique with different membrane receptor profiles and basement membrane thickness from specific branching area to area, so as to regulate cell growth or differentiation sub-locally. [36] Important players include beta-1 integrin , epidermal growth factor receptor (EGFR), laminin-1/5 , collagen-IV , matrix metalloproteinase (MMPs), heparan sulfate proteoglycans , and others. Elevated circulating level of growth hormone and estrogen get to multipotent cap cells on TEB tips through a thin, leaky layer of basement membrane. These hormones promote specific gene expression. Hence cap cells can differentiate into myoepithelial and luminal (duct) epithelial cells, and the increased amount of activated MMPs can degrade surrounding ECM helping duct buds to reach further in the fat pads. [37] [38] On the other hand, basement membrane along the mature mammary ducts is thicker, with strong adhesion to epithelial cells via binding to integrin and non-integrin receptors. When side branches develop, it is a much more “pushing-forward” working process including extending through myoepithelial cells, degrading basement membrane and then invading into a periductal layer of fibrous stromal tissue. [5] Degraded basement membrane fragments (laminin-5) roles to lead the way of mammary epithelial cells migration. [39] Whereas, laminin -1 interacts with non-integrin receptor dystroglycan negatively regulates this side branching process in case of cancer . [40] These complex "Yin-yang" balancing crosstalks between mammary ECM and epithelial cells "instruct" healthy mammary gland development until adult.

Which gland produces testosterone

which gland produces testosterone

Lactiferous duct development occurs in females in response to circulating hormones . First development is frequently seen during pre- and postnatal stages, and later during puberty . Estrogen promotes branching differentiation, [34] whereas in males testosterone inhibits it. A mature duct tree reaching the limit of the fat pad of the mammary gland comes into being by bifurcation of duct terminal end buds (TEB), secondary branches sprouting from primary ducts [5] [35] and proper duct lumen formation. These processes are tightly modulated by components of mammary epithelial ECM interacting with systemic hormones and local secreting factors. However, for each mechanism the epithelial cells' " niche " can be delicately unique with different membrane receptor profiles and basement membrane thickness from specific branching area to area, so as to regulate cell growth or differentiation sub-locally. [36] Important players include beta-1 integrin , epidermal growth factor receptor (EGFR), laminin-1/5 , collagen-IV , matrix metalloproteinase (MMPs), heparan sulfate proteoglycans , and others. Elevated circulating level of growth hormone and estrogen get to multipotent cap cells on TEB tips through a thin, leaky layer of basement membrane. These hormones promote specific gene expression. Hence cap cells can differentiate into myoepithelial and luminal (duct) epithelial cells, and the increased amount of activated MMPs can degrade surrounding ECM helping duct buds to reach further in the fat pads. [37] [38] On the other hand, basement membrane along the mature mammary ducts is thicker, with strong adhesion to epithelial cells via binding to integrin and non-integrin receptors. When side branches develop, it is a much more “pushing-forward” working process including extending through myoepithelial cells, degrading basement membrane and then invading into a periductal layer of fibrous stromal tissue. [5] Degraded basement membrane fragments (laminin-5) roles to lead the way of mammary epithelial cells migration. [39] Whereas, laminin -1 interacts with non-integrin receptor dystroglycan negatively regulates this side branching process in case of cancer . [40] These complex "Yin-yang" balancing crosstalks between mammary ECM and epithelial cells "instruct" healthy mammary gland development until adult.

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