Stimulates secretion of testosterone

In autoimmune gastritis , the immune system attacks the parietal cells leading to hypochlorhydria (low stomach acid secretion). This results in an elevated gastrin level in an attempt to compensate for increased pH in the stomach. Eventually, all the parietal cells are lost and achlorhydria results leading to a loss of negative feedback on gastrin secretion. Plasma gastrin concentration is elevated in virtually all individuals with mucolipidosis type IV (mean 1507 pg/mL; range 400-4100 pg/mL) (normal 0-200 pg/mL) secondary to a constitutive achlorhydria. This finding facilitates the diagnosis of patients with this neurogenetic disorder. [14] Additionally, elevated gastrin levels may be present in chronic gastritis resulting from H pylori infection. [15]

Type VI secretion systems were originally identified in 2006 by the group of John Mekalanos at the Harvard Medical School (Boston, USA) in two bacterial pathogens, Vibrio cholerae and Pseudomonas aeruginosa . [18] [19] These were identified when mutations in the Hcp and VrgG genes in Vibrio Cholerae led to decreased virulence and pathogenicity. Since then, Type VI secretion systems have been found in a quarter of all proteobacterial genomes, including animal, plant, human pathogens, as well as soil, environmental or marine bacteria. [20] [21] While most of the early studies of Type VI secretion focused on its role in the pathogenesis of higher organisms, more recent studies suggested a broader physiological role in defense against simple eukaryotic predators and its role in inter-bacteria interactions. [22] [23] The Type VI secretion system gene clusters contain from 15 to more than 20 genes, two of which, Hcp and VgrG, have been shown to be nearly universally secreted substrates of the system. Structural analysis of these and other proteins in this system bear a striking resemblance to the tail spike of the T4 phage, and the activity of the system is thought to functionally resemble phage infection. [24]

If the mono test is initially negative but the healthcare practitioner still suspects mono, a repeat test done a week or so later may be used to determine whether heterophile antibodies have developed. If the mono test is persistently negative, a test specific for EBV antibodies may be used to help confirm or rule out the presence of an EBV infection. A strep test may also be ordered along with a mono test to determine whether a person's sore throat is due to strep throat (group A streptococcal infection) instead of or in addition to mononucleosis.

Elegant studies from Wang and colleagues demonstrate that insulin induces activation of GABA(A) receptors in the alpha cells by GABA receptor translocation via an Akt kinase-dependent pathway. This leads to membrane hyperpolarization in the alpha cells and, ultimately, suppression of glucagon secretion. Hence, insulin may directly inhibit glucagon secretion, and indirectly potentiate the inhibitory effects of GABA concomitant released by β -cells-See Intra-islet insulin suppresses glucagon release via GABA-GABA(A) receptor system. Cell Metab. 2006 Jan;3(1):47-58

Diagnosis Index entries containing back-references to :

  • Antidiuretic hormone syndrome
  • Hypersecretion
    • hormone (s)
      • antidiuretic
  • Inappropriate
    • secretion
      • antidiuretic hormone (ADH) (excessive)
      • pituitary (posterior)
  • Increase, increased
    • function
      • pituitary (gland) (anterior) (lobe) ICD-10-CM Diagnosis Code Hyperfunction of pituitary gland, unspecified
          2016 2017 2018 Billable/Specific Code
        • posterior
  • Perversion, perverted
    • function
      • pituitary gland ICD-10-CM Diagnosis Code Diabetes insipidus
          2016 2017 2018 Billable/Specific Code
        Type 1 Excludes
        • nephrogenic diabetes insipidus ( )
        • posterior lobe
  • Schwartz-Bartter syndrome
  • Secretion
    • hormone
      • antidiuretic, inappropriate (syndrome)
    • antidiuretic hormone, inappropriate
  • Syndrome - see also Disease
    • inappropriate secretion of antidiuretic hormone
    • Schwartz-Bartter

Stimulates secretion of testosterone

stimulates secretion of testosterone

Elegant studies from Wang and colleagues demonstrate that insulin induces activation of GABA(A) receptors in the alpha cells by GABA receptor translocation via an Akt kinase-dependent pathway. This leads to membrane hyperpolarization in the alpha cells and, ultimately, suppression of glucagon secretion. Hence, insulin may directly inhibit glucagon secretion, and indirectly potentiate the inhibitory effects of GABA concomitant released by β -cells-See Intra-islet insulin suppresses glucagon release via GABA-GABA(A) receptor system. Cell Metab. 2006 Jan;3(1):47-58

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