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(physiology) processes that maintain a generally constant physiological state in a cell or organism

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/12/05 02:10:05」(JST)

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Autoregulation is a process within many biological systems, resulting from an internal adaptive mechanism that works to adjust (or mitigate) that system's response to stimuli. While most systems of the body show some degree of autoregulation, it is most clearly observed in the kidney, the heart, and the brain.^[1] Perfusion of these organs (especially the latter two) is essential for life, and through autoregulation the body can divert blood (and thus, oxygen) where it is most needed.

Cerebral autoregulation[edit]

More so than most other organs, the brain is very sensitive to overperfusion, and cerebral autoregulation plays an important role in maintaining an appropriate blood pressure to that region. Brain blood flow autoregulation is abolished when abnormally high CO2 levels persist. More detail is available at Cerebral perfusion pressure.

Homeometric autoregulation[edit]

Homeometric autoregulation, in the context of the circulatory system, is the heart's ability to increase contractility and restore stroke volume when afterload increases.^[2] This is in contrast to heterometric regulation.

Coronary circulatory autoregulation[edit]

Since the heart is a very aerobic organ, needing oxygen for the efficient production of ATP & Creatine Phosphate from fatty acids (and to a smaller extent, glucose & very little lactate), the coronary circulation is auto regulated so that the heart receives the right flow of blood & hence sufficient supply of oxygen. If a sufficient flow of oxygen is met and the resistance in the coronary circulation rises (perhaps due to vasoconstriction), then the coronary perfusion pressure (CPP) increases proportionally, to maintain the same flow. In this way, the same flow through the coronary circulation is maintained over a range of pressures. This part of coronary circulatory regulation is known as auto regulation and it occurs over a plateau, reflecting the constant blood flow at varying CPP & resistance. The slope of a CBF (coronary blood flow) vs. CPP graph gives 1/Resistance.

Renal autoregulation[edit]

There is "autoregulation" of renal blood flow and glomerular filtration rate in isolated kidneys. However it is likely that both these parameters change to some extent in vivo, e.g. hypotension, during exercise. Autoregulation is the relative independence, from systemic blood pressure, of glomerular filtration rate and renal blood flow over the physiological range of mean arterial pressure (c.80-180 mmHg)

Autoregulation of genes[edit]

This is so-called "steady-state system". An example is a system in which a protein a that is a product of gene A "positively regulates its own production by binding to a regulatory element of the gene coding for it"^[3] , and the protein gets used or lost at a rate that increases as its concentration increases. This feedback loop creates two possible states "on" and "off". If an outside factor makes the concentration of a increase to some threshold level, the production of protein a is "on", i.e. a will maintain its own concentration at a certain level, until some other stimulus will lower it down below the threshold level, when concentration of a will be insufficient to make gene A express at the rate that would overcome the loss or use of the protein a. This state ("on" or "off") gets inherited after cell division, since the concentration of protein a usually remains the same after mitosis. However, the state can be easily disrupted by outside factors. ^[3]

References[edit]

^ Autoregulation
^ Sarnoff SJ, Mitchell JH, Gilmore JP, Remensnyder JP (1960). "Homeometric autoregulation in the heart". Circulation Research 8 (5): 1077–1091. PMID 13746560.
^ ^a ^b Jablonka E., Lachmann M., Lamb M.J. (1992). "Evidence, Mechanisms and Models for the Inheritance of Acquired Characters". Journal of Theoretical Biology: 245–268.

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English Journal

Expression and Purification of Optimized rolGLP-1, A Novel GLP-1 Analog, in Escherichia Coli BL21(DE3) and its Good Glucoregulatory Effect on Type 2 Diabetic Mice.

Ma B, Tu P, Zhao X, Zhang Y, Wang Y, Ma C, Ji Y, Li X, Abbas SA, Li M.Author information Key Laboratory for Bioactive Materials of the Ministry of Education, Institute of Molecular Biology, College of Life Science, Nankai University, Tianjin 300071, P.R. China. mgl@nankai.edu.cn.AbstractGlucagon-like peptide-1 (GLP-1) is an incretin hormone that decreases postprandial glycemic excursions by enhancing insulin secretion but with short half-life due to rapid inactivation by enzymatic N-terminal truncation. Therefore, efforts are being made to improve the stability of GLP-1 via modifying its structure or inhibiting dipeptidylpeptidase IV (DPP IV), which is responsible for its degradation. GLP-M, consisting of 10 tandem repeated rolGLP-1 (GLP-1 analog), has been expressed in Pichia pastoris by our laboratory. Although it had a long effect of maintaining glucose homeostasis, redundant amino acids and purification tag limited its application. Here, optimized rolGLP-1(GLPO) with no redundant amino acids and purification tag was constructed by molecular cloning and site-directed mutagenesis, which was expressed efficiently in Escherichia coli BL21(DE3) with the production of 81.5 mg/L, and confirmed by the results of SDS-PAGE electrophoresis and Western Blotting. Then GLP-O was purified via ion exchange chromatography and gel filtration chromatography. The purity of GLP-O was close to 100%. GLP-O could be cut into single rolGLP-1 by trypsin in vitro, and rolGLP-1 had anti-trypsin activity. After oral administration of GLP-O for 4 weeks, the level of blood glucose in type 2 diabetic mice was lowered effectively, and the oral glucose tolerance of mice was improved significantly. These results settled the foundation for further clinical application of GLP-O.
Current pharmaceutical biotechnology.Curr Pharm Biotechnol.2014 Nov;14(11):985-94.
Glucagon-like peptide-1 (GLP-1) is an incretin hormone that decreases postprandial glycemic excursions by enhancing insulin secretion but with short half-life due to rapid inactivation by enzymatic N-terminal truncation. Therefore, efforts are being made to improve the stability of GLP-1 via modifyi
PMID 24372241

Friendly pathogens: prevent or provoke autoimmunity.

Sathyabama S, Khan N, Agrewala JN.Author information CSIR Institute of Microbial Technology , Chandigarh , India.AbstractAbstract The gut microflora is an immense health asset for human beings. The mammalian gut harbors trillions of commensals. These microbes not only modulate local but also systemic immunity. Recently, various reports are evolving, which signify that the gut microbes can modulate, tune and tame the host immune response. Consequently, it advocates the significance of the microbial composition. Further, the microbiota provides a fine equilibrium to host by regulating immune homeostasis. Furthermore, disturbance in this population can incite imbalance in immune system, leading to molecular mimicry and therefore autoimmunity. Hence, it is imperative to understand the influence of these bugs in preventing or provoking immune system against the self-components. In this article, we highlight the interaction between different gut microbes and cells of immune system and the mechanism involved in controlling and curtailing various autoimmune diseases.
Critical reviews in microbiology.Crit Rev Microbiol.2014 Aug;40(3):273-80. doi: 10.3109/1040841X.2013.787043. Epub 2013 May 21.
Abstract The gut microflora is an immense health asset for human beings. The mammalian gut harbors trillions of commensals. These microbes not only modulate local but also systemic immunity. Recently, various reports are evolving, which signify that the gut microbes can modulate, tune and tame the h
PMID 23688247

In Vivo Deletion of CAR Resulted in High Bone Mass Phenotypes in Male Mice.

Cho HY, Jung JY, Park H, Yang JY, Jung S, An JH, Cho SW, Kim SW, Kim SY, Kim JE, Park YJ, Shin CS.Author information Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.AbstractConstitutive androstane receptor (CAR) was originally identified as xenobiotic sensor that regulates the expression of cytochrome P450 genes. However, recent studies suggest that this nuclear receptor is also involved in the regulation of energy metabolism including glucose and lipid homeostasis. This study investigated the role of CAR in the regulation of bone mass in vivo using CAR(-/-) mice. Endogenous mRNA expression of CAR was observed in both primary osteoblasts and osteoclast precursors. CAR(-/-) mice have exhibited significant increase in whole body bone mineral density (BMD) by 9.5% (P < 0.01) and 5.5% (P < 0.05) at 10 and 15 weeks of age, respectively, compared with WT mice in males. Microcomputed tomography analysis of proximal tibia demonstrated a significant increase in trabecular bone volume (62.7%), trabecular number (54.1%) in male CAR(-/-) mice compared with WT mice. However, primary culture of calvarial cells exhibited no significant changes in osteogenic differentiation potential between CAR(-/-) and WT. In addition, the number of tartrate-resistant acid-phosphatase positive osteoclasts in the femur and serum level of CTx was not different between CAR(-/-) and WT mice. The higher BMD and microstructural parameters were not observed in female mice. Interestingly, serum level of testosterone in male CAR(-/-) mice was 2.5-fold higher compared with WT mice and the mRNA expressions of Cyp2b9 and 2b10 in the liver, which regulate testosterone metabolism, were significantly down-regulated in male CAR(-/-) mice. Furthermore, the difference in BMD between CAR(-/-) and WT mice disappeared at 8 weeks after performing orchiectomy. CAR(-/-) mice also exhibited significant increase in serum 1,25(OH)2 D3 levels but Cyp 27B1 which converts 25(OH)D3 to 1,25(OH)2 D3 was significantly down-regulated compared to WT mice. These results suggest that in vivo deletion of CAR resulted in higher bone mass, which appears to be a result from reduced metabolism of testosterone due to down-regulation of Cyp2b. J. Cell. Physiol. 229: 561-571, 2014. © 2013 Wiley Periodicals, Inc.
Journal of cellular physiology.J Cell Physiol.2014 May;229(5):561-71. doi: 10.1002/jcp.24478.
Constitutive androstane receptor (CAR) was originally identified as xenobiotic sensor that regulates the expression of cytochrome P450 genes. However, recent studies suggest that this nuclear receptor is also involved in the regulation of energy metabolism including glucose and lipid homeostasis. Th
PMID 24114688