Role of Microtubules in the Phasic Pattern of Insulin Release*

Malaisse, Willy; Malaisse‐Lagae, Francine; Obberghen, Emmanuel Van; Somers, Guido; Devis, Ghislain; Ravazzola, Mariella; Orci, Lelio

doi:10.1111/j.1749-6632.1975.tb19234.x

Cited by 131 publications

(58 citation statements)

References 47 publications

(8 reference statements)

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“…In designing this experiment, we took into account the time-and dose-related effect of mitotic spindleinhibitors upon the B-cell microtubular apparatus (23), so that the labeling of the islets occurred at a time (Table I). It fell slightly during the second incubation (120th-210th min) to 79.4+7.4% of its initial paired value.…”

Section: Resultsmentioning

confidence: 99%

Role of microtubules in the synthesis, conversion, and release of (pro)insulin. A biochemical and radioautographic study in rat islets.

Malaisse‐Lagae¹,

Amherdt²,

Ravazzola³

et al. 1979

J. Clin. Invest.

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A B S T R A C T In the pancreatic B cell, microtubules are thought to be involved in the process of insulin release. Their possible participation in the sequence of events leading from the biosynthesis and conversion of proinsulin to the release of newly synthesized insulin was investigated in rat isolated islets exposed to colchicine (0.1 mM). When the islets were preincubated for 30 min with colchicine and [3H]-leucine and, thereafter, incubated for two successive periods of 90 min each, still in the presence of colchicine, the release of preformed insulin was progressively inhibited and that ofnewly synthesized hormone delayed. When the islets were preincubated for 120 min with colchicine, subsequently pulse-labeled with [3H]leucine, and eventually examined by ultrastructural autoradiography, the export of newly synthesized proinsulin out of the rough endoplasmic reticulum, its transit through the Golgi complex, and its eventual packaging in secretory granules were all retarded. This situation was associated with a delayed conversion of proinsulin to insulin. Under the same experimental conditions, colchicine failed to affect the oxidation of glucose and adenylate charge in the islets. The effect of colchicine upon the release of preformed and newly synthesized insulin was not reproduced by lumicolchicine. It is concluded that colchicine interferes with the system controlling the intracellular transfer of secretory material from site of synthesis to site of release. This interference is likely to be linked to the effect of colchicine on microtubules.Parts of this work were reported in a preliminary form (1, 2).Receivedfor publication 19June 1978 and in revised form 22 Januarti 1979.

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Section: Resultsmentioning

confidence: 99%

Role of microtubules in the synthesis, conversion, and release of (pro)insulin. A biochemical and radioautographic study in rat islets.

Malaisse‐Lagae¹,

Amherdt²,

Ravazzola³

et al. 1979

J. Clin. Invest.

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“…It has been reported that colchicine blocks the cyclooxygenase-2 (COX-2) activity, prostaglandin E 2 and thromboxane A 2 synthesis of mononuclear phagocytes with subsequent reduction of swelling and pain in gout and Familial Mediterranean Fever (FMF) (Pouliot et al, 1998). In addition, this colchicine is known for tyrosine phosphorylation and superoxide anion production inhibitor (Roberge et al, 1996), arachidonate release and 5-lipoxygenase inhibition (Peters-Golden et al, 1996;Zurier et al, 1973), histamine inhibition (Mekori et al, 1989), insulin and parathomone release (Gillespie et al, 1968;Malaisse et al, 1975). Colchicine at high dose causes bone marrow failure, skin eruption, nettle rash, stomatitis and intestinal bleeding.…”

Section: Introductionmentioning

confidence: 99%

Isolation and anti-inflammatory activity of colchicinoids fromGloriosa superbaseeds

Joshi

Ekambaram

Mathela

2009

Pharmaceutical Biology

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“…3 " 5 We have also shown that vincristine and colchicine inhibit glucose-induced insulin release in vivo. 6 - 7 However, our recent studies 8 - 9 have shown that in the intact rat: (1) vincristine caused inhibition of glucose-induced insulin release in the presence or absence of morphologic disruption of the beta-cell microtubules; but, in contrast, (2) vincristine failed to inhibit arginine-induced insulin release either in the presence or absence of the beta-cell microtubular disruption.…”

mentioning

confidence: 83%

Glucose but not Arginine Prevents the Inhibitory Effect of Vincristine on Glucose-induced Insulin Release

et al. 1982

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SUMMARYWe have previously shown that in the intact rat: (1) the inhibition of glucose-induced insulin release caused by vincristine occurred in the presence or absence of morphologic disruption of the beta-cell microtubules; and (2) vincristine, however, failed to inhibit arginine-induced insulin release, even in the presence of a marked disruption of the beta-cell microtubules. The present study further evaluated the mechanism of inhibition of vincristine on glucose-induced insulin release in the intact rat. In the first series of studies, glucose (500 mg/kg) was infused over 1 min into fasting rats with indwelling vascular catheters. Five minutes later, vincristine (0.15 mg/kg i.v.) or vehicle (control) was injected. Sixty minutes after vincristine or vehicle treatment, insulin release in response to a 150-mg i.v. glucose pulse was examined. Serum insulin and glucose levels were similar at all time intervals in the vincristine-treated and the control rats. In the next series of studies, the experiments were repeated as above, except arginine (100 mg/kg), instead of glucose, was infused over 1 min before vincristine or vehicle treatment. In these studies, serum insulin in response to a glucose pulse was significantly inhibited in the vincristine-treated rats as compared with control rats. Therefore, in the intact rat, prior exposure to glucose but not arginine protected the beta-cell from the inhibitory effect of vincristine on glucose-induced insulin release. These findings, along with our previous observations, support the concept that arginine-induced insulin release is mediated via mechanisms other than those involved in glucose-induced insulin release and suggest that the in vivo effect of vincristine on glucose-induced insulin release is mediated via alteration of the beta-cell glucose receptors rather than microtubular structures. DIABETES

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Role of Microtubules in the Phasic Pattern of Insulin Release*

Cited by 131 publications

References 47 publications

Role of microtubules in the synthesis, conversion, and release of (pro)insulin. A biochemical and radioautographic study in rat islets.

Role of microtubules in the synthesis, conversion, and release of (pro)insulin. A biochemical and radioautographic study in rat islets.

Isolation and anti-inflammatory activity of colchicinoids fromGloriosa superbaseeds

Glucose but not Arginine Prevents the Inhibitory Effect of Vincristine on Glucose-induced Insulin Release

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