INSULIN SECRETION ACUTE PICK TEST AND RENAL TEST OF HYPERINSULINEMIA-INSULINRESISTANCE.

tag:blogger.com,1999:blog-2695693265049490064.post-25577574237822403652009-04-16T09:12:00.000-07:002009-04-16T09:13:53.038-07:00INSULIN SECRETION ACUTE PICK TEST AND RENAL TEST OF HYPERINSULINEMIA-INSULINRESISTANCE.<a name="_Toc60654054"></a><a name="_Toc60654029">Introduction.</a><o:p></o:p> Since decades, it is generally admitted that insulin represents an hormone or signal, which comunicates to muscular, hepatic and adipose cells the information necessary to blood glucose up-take, and utilize it in order to produce energy, unavoidable to survival.<o:p></o:p> As regards Quantum-Biophysical Semeiotics and especially Clinical Microangiology, “endogenous” insulin, obtained by the acute pick test of insulin secretion, is useful, due to its different and opposite action on tissue-microvascular unit of various biological systems under physiological and pathological conditions, even if the later are initial or early or “potential”, as demonstrates the particular microcirculatory activation in post-absorptive state as well as in absorptive state, described previously (See <a href="http://www.semeioticabiofisica.it/">www.semeioticabiofisica.it</a>, and the linked website <a href="www.Microangiology.it">www.Microangiology.it</a>).<o:p></o:p> Really, insulin is also a growth-factor, which modulates proteasomic activity and stimulates ILGF1-receptors, beeng active similarly on parenchyma and related microcircle.<o:p></o:p> Analogously to GH, as I demonstrated clinically (See Bibliography in the site), in both tissues at “real” risk for disease, i.e., in the so-called pre-morbid-stage, grew zone, pre-metabolic syndrome and in initial or light morbid phase, without any clinical phenomenology, the acute pick test of insulin secretion provokes exclusively the increase of arteriolar blood-flow and, thus, “opening” of AVA, functionally speaking (EBD obviously appear “closed” for a time longer than normal under similar conditions) and, then, it follows that there is microcirculatory activation, dissociated, type II or III (intermediate), i.e., increased vasomotility, but contemporaneously reduced or respectively “normal” vasomotion (1-13), so that it is present the dangerous micorcirculatory phenomenon of the “centralization” of blood-flow, more or less severe, throughout microvessels. <o:p></o:p> Such as pathological phenomenon accounts for the reason that tissue O2 as well as locale pH are reduced, as doctor can assess in a quantitative manner by Quantum-Biophysical Semeiotics: both gastric aspecific and caecal reflex show a reduced latency time, a prolonged duration (³ 4 sec.) and lowered differential lt (= reduced fractal dimension of both tissue and microvascular non-linear dynamics of the studied biological system), while choledocic reflex , i.e. choledocic contraction, during apnea test shows a duration lasting more than the physiological one (NN > 3 < style=""> fD).<o:p></o:p> Once again, these parameters values underscore the internal and external coherence of the biophysical-semeiotic theory, to which we shall come back often, due to its epistemological significance: as we have really frequently stated, internal and external coherence of whatever scientific theory does not surely coincide with its “thrut”, but it represents the conditio sine qua non of such as thrut.<o:p></o:p> <o:p> </o:p> <a name="_Toc60654055"></a><a name="_Toc60654030">Insulin Microvascular Action Mechanisms: Insulin-Secretion Acute Pick Test.</a><o:p></o:p> <o:p> </o:p> The dual effect of insulin through receptor activation is nowadays generally admitted, as follows: one is based on the insulin receptor substrates (IRSs); the other goes through a different class of molecules known as Shc, which leads to the activation of the mitogen-activated protein kinase (MAPK) pathway. Under insulin resistance condition, there is a pro-atherogenic effect that is mediated through activation of MAPK activated by the increased insulin levels, while the non-atherogenic pathway through phosphatidylinositide-3-kinase (PI3-kinase) activation, responsible for glucose transport, as well as nitric oxide (NO)-mediated-vasodilation are attenuated. Activation of the angiotensin II receptor further magnifies the pro-atherogenic effect (14). Since now, we can understand already the real reason of vasoconstriction brought about by insulin in presence of insulin-resistance. <o:p></o:p> In other words, insulin-dependent “pathological” vasocostriction parallels insulin-resistance. In addition, although the majority of patients with IGT have the metabolic syndrome (IIR), the latter can also be present in individuals before they develop IGT (14), i.e., in the Pre-Metabolic Syndrome, possibly evolving to Metabolic Syndrome, as I suggested previously, for long time (See the linked website <a href="www.microangiology.it">www.microangiology.it</a>: Pre-Metabolic Syndrome). <o:p></o:p> At this point, one must consider the primary role played by central adiposity in the occurrence of IIR and pre-metabolic and metabolic syndrome, all authors agree with. Patients with insulin resistance have low adiponectin levels that can improve, e.g., after weight loss (See <a href="http://www.semeioticabiofisica.it/">www.semeioticabiofisica.it</a>, Practical Applications). Resistin, another adipokine, appears to antagonize the effects of insulin on glucose homeostasis and to contribute to insulin resistance in animals (15) Further studies are necessary to clarify the role in human physiology and pathophysiology. Abdominal or visceral fat cells are also responsible for the formation and release of toxic proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and serum amyloid A (16). These cytokines contribute to insulin resistance and play an important role in accelerating the atherogenic process. Finally, central adiposity is also associated with high levels of PAI-1, causing impaired fibrinolysis and contributing to the development and progression of CVD (16).<o:p></o:p> In diseased parenchymas, even seemingly healthy from the clinical view-point, insulin induces tissue-microvascular modifications of great diagnostic importance: for instance, digital “light-moderate” pressure, applied on whatever joint at “real” risk of rheumatic disease or, of course, involved slightly or initially by a form of connectivitis, e.g., causes the occurrence of deterministic chaotic fluctuations of both upper and lower ureteral reflexes, showing a fD of 3,81, or slightly altered. <o:p></o:p> In other words, both vasomotility and vasomotion appear to be apparently normal or show really slight modification, so that rheumo-gastric aspecific reflex and/or caecal reflex latency time results only slight reduced or normal (NN = 8 sec.), reflex duration slight prolonged, i.e., ³ 4 sec. (NN <> 4 sec.: f D = 3,8).<o:p></o:p> By contrast, after the acute pick of insulin secretion, under above-mentioned pre-morbid situation, we observe intense microcirculatory modifications of “vasomotion”, i.e., blood-flow “centralization”, reduced blood supply to parenchyma, and consequently histangic acidosis, which brings about reduced insulin- as well as adrenergic-receptors sensitivity.<o:p></o:p> In other words, the secretion of acute insulin pick displays the “latent” abnormality of Microcirculatory Functional Reserve in biological systems or their regions, in which there is not at this moment any disorders, causing a behaviour changing similar to that induced by biophysical- semeiotic preconditioning (See Glossary in the website <a href="http://www.semeioticabiofisica.it/">www.semeioticabiofisica.it</a>), which is a clinical tool really efficacious in the research, diagnosis, and therapeutic monitoring. Such as topic has been in detail discussed in former article in the site <a href="http://www.microangiologia.it/">www.microangiologia.it</a>. <o:p></o:p> Other numerous applications of this test provide doctor bed-side useful information, allowing the refined investigation of all biological systems, starting from the potential or initial stages of the local disorder, for instance, in “real risk” of malignancy. <o:p></o:p> <o:p> </o:p> In healthy, digital pressure applied on radial artery is followed by occurrence of “in toto” ureteral reflex, <st1:metricconverter productid="1 cm" st="on">1 cm</st1:metricconverter>. in intensity, which increases after the test illustrated above: normal arterial compliance.<o:p></o:p> On the contrary, in case of reduced arterial compliance, as it happens, e.g., in both arterial hypertension and arteriosclerosis, starting from the stage of “real” risk, i.e., early stage, characterized generally by hyperinsulinemia-insulinresistance, detected by Quantum-Biophysical Semeiotics, basal “in toto” ureteral reflex is < <st1:metricconverter productid="1 cm" st="on">1 cm</st1:metricconverter>. and it lowers after insulin secretion acute pick test, due to pathological vasoconstriction (17-20).<o:p></o:p> Notoriously, under such as conditions the hormone brings about negative phenomena in micro-and macro-vessels, characterized by “vasospasm”, as consequence of the increase of PKC as well as of free oxygen radicals. caused by insulin in pathological conditions, even initial, as grew , pre-morbid stage or grew zone. It is a matter of vessel behaviour similar to that observed in case of acetyl-choline, which in healthy dilates the arteries, while in presence of functional or structural endothelial damage brings about notoriously vasospasm.<o:p></o:p> <o:p> </o:p> In conclusion, both tissue and microvascular response to transitory endogenous jatrogenetic hyperinsulinemia is really different in healthy subject, in individual at “inherited real risk” of degenerative, metabolic or oncological disease (See biophysical constitutions in the first website) and, of course, in diseased subject, even in absence of clinical phenomenology, as consequence of diverse receptor response to the hormone under different conditions.<o:p></o:p> <o:p> </o:p> <o:p> </o:p> <table class="MsoNormalTable" style="border: medium none ; border-collapse: collapse;" border="1" cellpadding="0" cellspacing="0"> <tbody><tr style=""> <td style="border: 1pt solid windowtext; padding: 0cm 3.5pt; width: 488.9pt;" valign="top" width="652"> Therefore, it is possible to utilize the twofold behaviour of biological systems in case of increased insulin blood level (insulin secretion acute pick test) aiming to diagnosis and prevention, utilizing the different, opposite, receptors responsiveness of smooth muscle cells to insulin, but also to catecholamines (apnea test or Restano’s manoeuvre) as well as to acetylcholine (Valsalsa’s manoeuvre)<o:p></o:p> </td> </tr> </tbody></table> <o:p> </o:p> From the above remarks, it appears clear the patho-physiology of histangic ph lowering during the test, where whatever diease is already present or it will occur.<o:p></o:p> <o:p> </o:p> <table class="MsoNormalTable" style="border: medium none ; border-collapse: collapse;" border="1" cellpadding="0" cellspacing="0"> <tbody><tr style=""> <td style="border: 1pt solid windowtext; padding: 0cm 3.5pt; width: 488.9pt;" valign="top" width="652"> Consequently, it is not surprising our opinion, based on a long clinical experience, that CAEMH-a represents the conditio sine qua non of most common and dangerous human diseases: DM, Dyslipidemia, ATS, Rheumatic disorders, malignancies, Arteral Hypertension, a.s.o. <o:p></o:p> </td> </tr> </tbody></table> <o:p> </o:p> The relation, we demonstrated “clinically” and surely existent, between insulin and sympathetic nervous system, as well as that between hyperinsulinemia and insulinresistance, is not nowadays interpreted in the same way by the authors. In other words, authors do not agree on the primary cause between the two hormonal alterations.<o:p></o:p> <o:p></o:p> The following biophysical-semeiotic experimental evidence – “insulin secretion acute pick test” – demonstrates, in healthy, that jatrogenetic hyperinsulinemia is immediately followed by type I, associated microcirculatory activation of supra-renal gland (AL + PL = 8 sec.) and, then, by “sympathetic hypertonus”, event on which all authors agree, and we demonstrated by sophysticated semeiotics: lower mesenteric plexus-caecal reflex (= in practice, digital pressure on the area below umbelicus, slightly at right) shows a basal duration > 10 sec. (NN = 10 sec.). In fact, under normal condition, digital pressure brings about caecal dilation of about <st1:metricconverter productid="3 cm" st="on">3 cm</st1:metricconverter>., lasting 10 sec. exactly.<o:p></o:p> By contrast, after 10 sec. from the beginning of Restano’s manoeuvre (= sympathetyc hypertonus: see Glossary) reflex duration is > 10 sec. due to sympathetic hypertonus, while after 7-10 sec. from Valsalva’s manoeuvre starting the duration of caecal dilation lowers significantly to <></o:p> <o:p> </o:p> To summarize, hyperinsulinemia, beside all other actions, provokes notoriously sympathetic hypertonus, as allows us to state Quantum-Biophysiacal Semeiotics. On the other site, the stimulation of supra-renal trigger-point (the skin of hypocondrium immediately below the costal arch along anterior ascellar line) brings about increasing of supra-renal gland volume, and successively that pancreatic one, with subsequent augmentation of insular hormonal secretion.<o:p></o:p> <o:p> </o:p> The data, referred above, demonstrate that both biological systems activate each other reciprocally by positive feed-back mechanisms. At this point, however, in health, the positive arm of the “biological cross” of psycho-neuro-endocrine-immunological system, i.e., SST, melatonin, endogenous oppioids, which controls insulin, epinephrine and nor-epinephrine secretion, leading it in normal ranges in an opposite way to that occurs in presence of “Oncological Terrain” (See Oncological Terrain in my above-cited website). <o:p></o:p> With regards to this argument, it is useful to underline the importance of dismetabolic-dishormonal components – hyperinsulinemia-insulinresistance – as well as that of sympathetic hypertonus in the pathological pre-morbid condition, I termed “Oncological Terrain”.<o:p></o:p> <o:p> </o:p> <a name="_Toc60654056"></a><a name="_Toc60654031">Hyperinsulinemia-Insulinresistance Renal Test.</a><o:p></o:p> <o:p> </o:p> As follows, it is described a further interesting and reliable test to evaluate hyperinsulinemia-insulinresistance: hyperinsulinemia-insulinresistance renal test (See Glossary in above-cited website).<o:p></o:p> In health, acute pick of insulin secretion, performed as illustrated formerly, after a latency time < productid="3 cm" st="on">3 cm</st1:metricconverter>. with duration of 10 sec. precisely.<o:p></o:p> “Vasomotion” duration last (AL + PL Phase) 8 sec. (NN = 6 sec.), analogously to what we observe during the atrial natriuretic peptides renal test (See above-cited website in Practical Application).<o:p></o:p> Similarly to what doctor observes in both cardiac failure and coronary artery disease, as regards “atrial” natriuretic peptides, due to renal receptors down-regulation, the physiological increasing of kidney augmentation during acute pick of insulin secretion test appears to be slightest, not significant, very short or absent (= intensity < <st1:metricconverter productid="2 cm" st="on">2 cm</st1:metricconverter>. and duration £ 8 sec.), allowing bed-side assessment of a pathological situation, really dangerous, and otherwise impossible to be recognized, because it is at the moment completely asymptomatic: hyperinsulinemia-insulinresistance.<o:p></o:p> Moreover, the “quantitative” evaluation of increasing lt of renal diameters during the performance of acute pick insulin secretion test as well as augmentation rate of kidney size permit to “quantify” the seriousness of underlying pathological disorder.<o:p></o:p> In conclusion, renal test of hyperinsulinemia-insulin resistance results both quantitatively and qualitatively “abnormal” in disorders, even initial, of glucose metabolism: in Diabetes Mellitus, kidney does not increase the size or the increase of their diameters is not at all significant from the statistical view-point.<o:p></o:p> <o:p> </o:p> <a name="_Toc60654057"></a><a name="_Toc60654032">References.</a> <o:p> </o:p> 1) Stagnaro-Neri M., Stagnaro S. Indagine clinica percusso-ascoltatoria delle unità microvascolotessutali della plica ungueale. Acta Med. Medit. 4, 91 ,1988. 2) Stagnaro-Neri M., Stagnaro S., Auscultatory Percussion Evaluation of Arterio-venous Anastomoses Dysfunction in early Arteriosclerosis. Acta Med. Medit. 5, 141, 1989 3) Stagnaro-Neri M., Stagnaro S., Il Glutatione nella terapia microvascolare. Act Med. Medit. 7, 11, 1991<o:p></o:p> 4) Stagnaro-Neri M., Stagnaro S., Sul meccanismo d’azione di Sulodexide a livello di correlazioni istangiche acrali patologicamente alterate: studio clinico percusso-ascoltatorio. Giornate Naz. di Angiologia. Milano, 23-29 Giugno 1991. Atti Min. Med., 40, 1991 (Infotrieve) 5) Stagnaro S., Stagnaro-Neri M. Il danno da radicali liberi sul microcircolo. Congr. Naz. SISM., Milano, 10 giugno 1991, Comun. Atti, Min. Angiologica (Suppl. 1 al N° 1) 16,398, 1991. <o:p></o:p> 6) Stagnaro-Neri M., Stagnaro S., Modificazioni della viscosità ematica totale e della riserva funzionale microcircolatoria in individui a rischio di arteriosclerosi valutate con la percussione ascoltata durante lavoro muscolare isometrico. Acta Med. Medit. 6, 131-136, 1990. 7) Stagnaro S., Stagnaro-Neri M., Basi microcircolatorie della semeiotica biofisica. Atti del XVII Cong. Naz. Soc. Ital. Studio Microcircolazione, Firenze ott. 1995, Biblioteca Scient. Scuola Sanità Militare, 1995, 2, 94.<o:p></o:p> 8) Stagnaro S., Stagnaro-Neri M., Il test della Apnea nella Valutazione della Microcircolazione cerebrale in Cefalalgici. Atti, Congr. Naz. Soc. Ita. Microangiologia e Microcircolazione. A cura di C. Allegra. Pg. 457, Roma 10-13 Settembre 1987. Monduzzi Ed. Bologna, 1987.<o:p></o:p> 9) Stagnaro S., Valutazione percusso-ascoltatoria della microcircolazione cerebrale globale e regionale. Atti, XII Congr. Naz. Soc. It. di Microangiologia e Microcircolazione. 13-15 Ottobre, <st1:city st="on"><st1:place st="on">Salerno</st1:place></st1:City>, e Acta Medit. 145, 163, 1986.<o:p></o:p> 10) Stagnaro-Neri M., Stagnaro S., Deterministic chaotic biological system: the microcirculatoory bed. Theoretical and practical aspects. Gazz. Med. It. – Arch. Sc. Med. 153, 99, 1994.<o:p></o:p> 11) Stagnaro-Neri M., Stagnaro S., Radicali liberi e alterazioni del microcircolo nelle flebopatie ipotoniche costituzionali. Min. Angiol. 18, Suppl. 2 al N. 4, 105, 1993.<o:p></o:p> 12) Stagnaro S., Stagnaro-Neri M. Il danno da radicali liberi sul microcircolo. Congr. Naz. SISM., Milano, 10 giugno 1991, Comun. Atti, Min. Angiologica (Suppl. 1 al N° 1) 16,398. 1991.<o:p></o:p> 13) Stagnaro-Neri M., Stagnaro S. Introduzione alla Semeiotica Biofisica. Il Terreno Oncologico. Travel Factory, Roma, in stampa. <o:p></o:p> 14) Pantaleo A., Zonszein J. Using Insulin as a Drug Rather Than as a Replacement Hormone During Acute Illness: A New Paradigm, <a href="http://www.medscape.com/viewarticle/463524_print">http://www.medscape.com/viewarticle/463524_print</a> , Heart Dis 5(5):323-334, 2003.<o:p></o:p> 15) Janke J, Engeli S, Gorzelniak K, et al. Resistin gene expression in human adipocytes is not related to insulin resistance. Obes Res. 2002;10:1-5.<o:p></o:p> 16) Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest. 2000;106:473-481. <o:p></o:p> 17) Stagnaro S., <st1:place st="on">West PJ.</st1:place>, Hu FB., Manson JE., Willett WC. Diet and Risk of Type 2 Diabetes. N Engl J Med. 2002 Jan 24;346(4):297-298. [Medline]<o:p></o:p> 18) Stagnaro Sergio. Newborn-pathological Endoarteriolar Blocking Devices in Diabetic and Dislipidaemic Constitution and Diabetes Primary Prevention. The Lancet. March 06 2007. <a href="http://www.thelancet.com/journals/lancet/article/PIIS0140673607603316/comments?totalcomments=1">http://www.thelancet.com/journals/lancet/article/PIIS0140673607603316/comments?totalcomments=1</a> SEE particularly URL: <a href="http://www.fceonline.it/docs/stagnaro.pdf">http://www.fceonline.it/docs/stagnaro.pdf</a><o:p></o:p> 19) Stagnaro S. Pre-metabolic syndrome: the real initial stage of metabolic-syndrome, type 2 diabetes and arteroscleropathy. Cardiovascular Diabetology 3:1 <a href="http://www.cardiab.com/content/3/1/1/comments">http://www.cardiab.com/content/3/1/1/comments</a><o:p></o:p> 20) Stagnaro Sergio. Bedside recognizing diabetics with or without CHD real risk or silent CHD. BMC Cardiovascular Disorders 2006, 6:41 <a href="http://www.biomedcentral.com/1471-2261/6/41/comments#243544">http://www.biomedcentral.com/1471-2261/6/41/comments#243544</a><o:p></o:p> <o:p> </o:p><div class="blogger-post-footer"><img width='1' height='1' src='https://blogger.googleusercontent.com/tracker/2695693265049490064-2557757423782240365?l=sciphu.com' alt='' /></div>Stagnarohttp://www.blogger.com/profile/12340616002338559392noreply@blogger.com0