Methods to Study the in vivo Regulation of Cyclic Nucleotides in Pituitary

2015 ◽  
pp. 197-205
Author(s):  
E. Costa ◽  
A. Guidotti ◽  
P. Uzunov ◽  
B. Zivkovic
Keyword(s):  
Cyclic Nucleotides

Hormonal regulation of canine intestinal cholesterol synthesis

1981 ◽  
Vol 240 (4) ◽  
pp. G274-G280
Author(s):  
M. W. Goodman ◽  
W. F. Prigge ◽  
R. L. Gebhard
Keyword(s):  
Cyclic Nucleotides ◽  
Hormonal Regulation ◽  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
In Vivo Studies ◽  
Synthesis Rate ◽  
Ileal Mucosa ◽  
Control Activity

Hormonal regulation of intestinal cholesterol synthesis was studied both in vitro and in vivo. Cholesterol synthesis rate was determined by measurement of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (EC 1.1.1.34) activity and by incorporation [14C]acetate into sterol. In vitro studies utilized organ culture of canine ileal mucosa. During 6-h culture, reductase activity was stimulated sevenfold. Insulin (10-6 M) augmented this rise to 144 +/- 7% of th control activity, while 10(-8) M glucagon, 10(-3) M adenosine 3',5'-cyclic monophosphate, and 3-isobutyl-1-methylxanthine suppressed activity (final reductase activity was 83 +/- 3%, 75 +/- 4%, and 41 +/- 3%, respectively, of cultured control values). In vivo studies utilized dogs with isolated Thiry-Vella ileal fistulas. In vivo, insulin doubled reductase activity while glucagon led to a 42 +/- 9% suppression. It is concluded that insulin and glucagon may be potential physiological regulators of intestinal cholesterol synthesis. The glucagon effect may be mediated by cyclic nucleotides.

scholarly journals Systems Biology Analysis Reveals Eight SLC22 Transporter Subgroups, Including OATs, OCTs, and OCTNs

2020 ◽  
Vol 21 (5) ◽  
pp. 1791 ◽  
Author(s):  
Darcy C. Engelhart ◽  
Jeffry C. Granados ◽  
Da Shi ◽  
Milton H. Saier Jr. ◽  
Michael E. Baker ◽  
...  
Keyword(s):  
Cyclic Nucleotides ◽  
Signaling Molecules ◽  
In Vitro Assays ◽  
Specific Substrate ◽  
In Vivo Models ◽  
Using Data ◽  
Carnitine Derivatives ◽  
Metabolite Network

The SLC22 family of OATs, OCTs, and OCTNs is emerging as a central hub of endogenous physiology. Despite often being referred to as “drug” transporters, they facilitate the movement of metabolites and key signaling molecules. An in-depth reanalysis supports a reassignment of these proteins into eight functional subgroups, with four new subgroups arising from the previously defined OAT subclade: OATS1 (SLC22A6, SLC22A8, and SLC22A20), OATS2 (SLC22A7), OATS3 (SLC22A11, SLC22A12, and Slc22a22), and OATS4 (SLC22A9, SLC22A10, SLC22A24, and SLC22A25). We propose merging the OCTN (SLC22A4, SLC22A5, and Slc22a21) and OCT-related (SLC22A15 and SLC22A16) subclades into the OCTN/OCTN-related subgroup. Using data from GWAS, in vivo models, and in vitro assays, we developed an SLC22 transporter-metabolite network and similar subgroup networks, which suggest how multiple SLC22 transporters with mono-, oligo-, and multi-specific substrate specificity interact to regulate metabolites. Subgroup associations include: OATS1 with signaling molecules, uremic toxins, and odorants, OATS2 with cyclic nucleotides, OATS3 with uric acid, OATS4 with conjugated sex hormones, particularly etiocholanolone glucuronide, OCT with neurotransmitters, and OCTN/OCTN-related with ergothioneine and carnitine derivatives. Our data suggest that the SLC22 family can work among itself, as well as with other ADME genes, to optimize levels of numerous metabolites and signaling molecules, involved in organ crosstalk and inter-organismal communication, as proposed by the remote sensing and signaling theory.

scholarly journals Sickling Cells, Cyclic Nucleotides, and Protein Kinases: The Pathophysiology of Urogenital Disorders in Sickle Cell Anemia

Anemia ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Mário Angelo Claudino ◽  
Kleber Yotsumoto Fertrin
Keyword(s):  
Protein Kinases ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Cyclic Nucleotides ◽  
Single Point ◽  
Clinical Manifestations ◽  
Single Point Mutation ◽  
Tract Infections

Sickle cell anemia is one of the best studied inherited diseases, and despite being caused by a single point mutation in theHBBgene, multiple pleiotropic effects of the abnormal hemoglobin S production range from vaso-occlusive crisis, stroke, and pulmonary hypertension to osteonecrosis and leg ulcers. Urogenital function is not spared, and although priapism is most frequently remembered, other related clinical manifestations have been described, such as nocturia, enuresis, increased frequence of lower urinary tract infections, urinary incontinence, hypogonadism, and testicular infarction. Studies on sickle cell vaso-occlusion and priapism using bothin vitroandin vivomodels have shed light on the pathogenesis of some of these events. The authors review what is known about the deleterious effects of sickling on the genitourinary tract and how the role of cyclic nucleotides signaling and protein kinases may help understand the pathophysiology underlying these manifestations and develop novel therapies in the setting of urogenital disorders in sickle cell disease.

Immuno-histochemical localization of cyclic nucleotides in mineralized tissues: Mechanically-stressed osteoblasts in vivo

1978 ◽  
Vol 192 (3) ◽  
pp. 363-373 ◽  
Author(s):  
Zeev Davidovitch ◽  
Paul C. Montgomery ◽  
Robert W. Yost ◽  
Joseph L. Shanfeld
Keyword(s):  
Cyclic Nucleotides ◽  
Histochemical Localization ◽  
Mineralized Tissues

ALTERATIONS IN CYCLIC NUCLEOTIDES IN DOGS AFTER TRIIODOTHYRONINE

1975 ◽  
Vol 79 (1) ◽  
pp. 66-75 ◽  
Author(s):  
J. A. Fernandez-Pol ◽  
Marguerite T. Hays
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Cyclic Nucleotides ◽  
Time Lag ◽  
The Other ◽  
Experimental Procedure ◽  
Single Intravenous Injection ◽  
Converse Relation

ABSTRACT The effects of triiodothyronine (T3) on plasma and tissue levels (liver, adipose tissue, muscle) of adenosine 3′,5′-monophosphate (cyclic AMP) and guanosine 3′,5′-monophosphate (cyclic GMP) were determined in Mongrel dogs. Plasma cyclic AMP increased to a mean plateau value 165 % greater than control values in response to a single intravenous injection of T3 (100–200 μg/kg body weight). This treatment resulted in no increase in plasma cyclic GMP. In liver, cyclic AMP concentration decreased 54 %, while cyclic GMP increased 137 %. Adipose tissue cyclic AMP levels decreased in control animals during the experimental procedure. On the other hand, animals given T3 had stable or (in one case) increasing adipose tissue cyclic AMP levels. Hence, T3, actually maintained higher levels than that expected, in comparison to the control. Cyclic GMP levels in adipose tissue were not affected by T3. Cyclic AMP and cyclic GMP were unchanged in muscle. In all cases, a time lag occurred (30–40 min) between administration of T3 and subsequent alterations in cyclic nucleotide levels. It was concluded that T3 is capable of altering concentrations of cyclic AMP and cyclic GMP in vivo and that cyclic AMP and cyclic GMP patterns of response are completely different. In liver, a converse relation of the two nucleotides is present. These findings are compatible with the hypothesis that some of T3's action may be explained by its effects upon either cyclic AMP or cyclic GMP.

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