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  1. Article: Effectiveness, Simplification and Persistence of IDegLira in Poorly Controlled People with Type 2 Diabetes: A 4-Year Follow-Up Real-World Study.

    Di Loreto, Chiara / Celleno, Roberta / Pezzuto, Debora / Ambrosi, Franca / Bellavita, Silvia / Biagini, Marinella / Passeri, Monica / Del Sindaco, Paola

    Diabetes therapy : research, treatment and education of diabetes and related disorders

    2024  

    Abstract: Introduction: Efficacy and safety of the fixed ratio combination of insulin degludec and liraglutide (IDegLira) has been largely documented. However, long-term data are limited. This study aimed at describing persistence in therapy and the effectiveness ...

    Abstract Introduction: Efficacy and safety of the fixed ratio combination of insulin degludec and liraglutide (IDegLira) has been largely documented. However, long-term data are limited. This study aimed at describing persistence in therapy and the effectiveness at 48 months of IDegLira.
    Methods: We conducted an observational study based on retrospective chart review. All patients treated with IDegLira during 2018-2022 were included. Data on treatment approaches and clinical outcomes were collected at the first prescription of IDegLira (T0) and after 6, 12, 24, 36, and 48 months.
    Results: Overall, 156 patients (mean age 68 years, 64.1% men) started IDegLira, of whom 88 (56.4%) were previously treated with basal-oral therapy (BOT) and 68 (43.6%) with basal-bolus schemes (BB). Before starting IDegLira, 23.8% were treated with ≥ 2 oral antihyperglycemic agents in association with insulin; at T0, the proportion decreased to 3.2%. Short-acting insulin was discontinued after the first week. After 48 months, levels of HbA1c were significantly reduced by 1.34% in the BOT group and 1.07% in the BB group (p < 0.0001 in both groups). In the BOT group, FBG levels decreased by about 50 mg/dl and body weight was unchanged. In the BB group, FBG levels decreased by about 40 mg/dl and body weight was significantly reduced by an average of 7.7 kg. Five patients (3.2%) interrupted therapy with IDegLira during 48 months, and no severe hypoglycemia occurred.
    Conclusions: Our study emphasizes the important role of IDegLira in maintaining a good metabolic control while minimizing the risk of major hypoglycemia and weight gain in the long term. The substantial simplification of treatment schemes can increase adherence.
    Language English
    Publishing date 2024-04-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2566702-6
    ISSN 1869-6961 ; 1869-6953
    ISSN (online) 1869-6961
    ISSN 1869-6953
    DOI 10.1007/s13300-024-01564-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Effects of S 21403 on hormone secretion from isolated rat pancreas at different glucose concentrations.

    Gregorio, Franco / Ambrosi, Franca / Boemi, Massimo / Carle, Flavia / Filipponi, Paolo

    European journal of pharmacology

    2002  Volume 456, Issue 1-3, Page(s) 141–147

    Abstract: We investigated the in vitro effects of therapeutical concentrations of S 21403 (a succinic acid derivative also known as KAD 1229 and mitiglinide) on insulin and glucagon secretion during a metabolic stimulus (glucose rising from 5 to 8.33 mM) or at a ... ...

    Abstract We investigated the in vitro effects of therapeutical concentrations of S 21403 (a succinic acid derivative also known as KAD 1229 and mitiglinide) on insulin and glucagon secretion during a metabolic stimulus (glucose rising from 5 to 8.33 mM) or at a stable 2.22 mM glucose using the isolated perfused rat pancreas model, and we compared them with the patterns of repaglinide and glibenclamide. Control perfusions were also performed. During 8.33 mM glucose, insulin release peaked to 339.12+/-22.87 microU/ml in controls. S 21403 enhanced insulin release (first peak 413.02+/-14.90 microU/ml; P<0.03 vs. controls, P=ns vs. repaglinide, P<0.005 vs. glibenclamide). Repaglinide increased glucose-induced first peak secretion to 409.33+/-20.05 microU/ml within the eighth minute (P<0.05 vs. controls, P<0.01 vs. glibenclamide). Glibenclamide did not affect the first phase of glucose-induced insulin release (peak of 338.41+/-29.79 microU/ml) but potentiated and delayed the second phase. No drug affected glucagon release. In conclusion, S 21403 induces a faster, more physiological pattern of insulin release than the other drugs we tested.
    MeSH term(s) Animals ; Carbamates/pharmacology ; Dose-Response Relationship, Drug ; Glucose/pharmacology ; Glyburide/pharmacology ; Hypoglycemic Agents/pharmacology ; In Vitro Techniques ; Indoles/pharmacology ; Insulin/metabolism ; Insulin Secretion ; Isoindoles ; Male ; Pancreas/drug effects ; Pancreas/metabolism ; Piperidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Time Factors
    Chemical Substances Carbamates ; Hypoglycemic Agents ; Indoles ; Insulin ; Isoindoles ; Piperidines ; repaglinide (668Z8C33LU) ; mitiglinide (D86I0XLB13) ; Glucose (IY9XDZ35W2) ; Glyburide (SX6K58TVWC)
    Language English
    Publishing date 2002-12-05
    Publishing country Netherlands
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/s0014-2999(02)02620-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Catecholamines and Pituitary Function

    Nicoletti, Ildo / Filipponi, Paolo / Fedeli, Leone / Sfrappini, Mario / Gregorini, Gregorio / Ambrosi, Franca / Santeusanio, Fausto

    Hormone Research - From Developmental Endocrinology to Clinical Research

    1984  Volume 20, Issue 3, Page(s) 202–212

    Abstract: Previous studies in Rhesus monkeys have demonstrated that a dopamine (DA) infusion rate of 0.1 μg/kg·min induces peripheral DA levels similar to those measured in hypophysial stalk blood and normalizes serum prolactin (PRL) levels in stalk-transected ... ...

    Abstract Previous studies in Rhesus monkeys have demonstrated that a dopamine (DA) infusion rate of 0.1 μg/kg·min induces peripheral DA levels similar to those measured in hypophysial stalk blood and normalizes serum prolactin (PRL) levels in stalk-transected animals. We therefore examined the effect of such DA infusion rate on basal and thyrotropin-releasing hormone (TRH)-stimulated PRL secretion in both normal cycling women and women with pathological hyperprolactinemia. 0.1 μg/kg·min DA infusion fully normalized PRL serum levels in 8 normal cycling women whose endogenous catecholamine synthesis had been inhibited by α-methyl-p-tyrosine (AMPT) pretreatment. Furthermore, DA significantly reduced, but did not abolish, the rise in serum PRL concentrations induced by both acute 500 mg AMPT administration and 200 μg intravenous TRH injection in normal women. A significant reduction in serum PRL levels in response to 0.1 μg/kg·min DA, similar to that observed in normal cycling women when expressed as a percentage of baseline PRL, was documented in 13 amenorrheic patients with TRH-unresponsive pathological hyperprolactinemia. However, a marked rise was observed in the serum PRL of the same patients when TRH was administered during the course of a 0.1-μg/kg·min DA infusion. The PRL response to TRH was significantly higher during DA than in basal conditions in hyperprolactinemic patients, irrespective of whether this was expressed as an absolute increase (Δ PRL 94.4 ± 14.2 vs. 17.8 ± 14.1 ng/ml, p < 0.002) or a percent increase (Δ% PRL 155.4 ± 18.9 vs. 17.9 ± 7.1, p < 0.0005), and there was a significant linear correlation between the PRL decrements induced by DA and the subsequent PRL responses to TRH. 1 A preliminary report of this investigation was presented at the National Meeting ‘Giornate Endocrinologiche Pisane’, Pisa, 1983. This research was supported in part by the Italian National Research Council (CNR) grant No. 82.02142. DA and TRH Interactions in the Control of PRL Release 203 These data would seem to show that the 0.1-μg/kg·min DA infusion rate reduces basal PRL secretion and blunts, but does not abolish, the PRL response to both TRH and acute AMPT administration. The strong reduction in PRL secretion and the restoration of the PRL response to TRH by 0.1 μg/kg·min DA infusion in the high majority of hyperprolactinemic patients, seem to indicate that both PRL hypersecretion and abnormal PRL response to TRH in women with pathological hyperprolactinemia are due to a relative DA deficiency at the DA receptor site of the pituitary lactotrophs.
    Keywords Hyperprolactinemia ; Dopamine infusion ; Catecholamine-synthesis inhibition ; Thyrotropin-releasing hormone ; Prolactin
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 124442-5
    ISSN 1423-0046 ; 0301-0163 ; 0301-0163
    ISSN (online) 1423-0046
    ISSN 0301-0163
    DOI 10.1159/000179997
    Database Karger publisher's database

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  4. Article: Catecholamines and Pituitary Function. VI. Effect of Different Dopamine Doses on TRH-Induced Prolactin Release in Women with Pathological Hyperprolactinemia

    Nicoletti, I. / Ambrosi, Franca / Pagliacci, Maria Cristina / Pelicci, Giuliana / Giammartino, C. / Maggio, D. / Fedeli, L. / Filipponi, P.

    Hormone and Metabolic Research

    1987  Volume 19, Issue 03, Page(s) 125–129

    Abstract: The present study was designed to examine the effect of low-dose dopamine (DA) infusion rates (0.02 and 0.1 μg/kg · min) on both basal and TRH-stimulated prolactin release in normal and hyperprolactinemic individuals. Sixteen normally menstruating women ... ...

    Abstract The present study was designed to examine the effect of low-dose dopamine (DA) infusion rates (0.02 and 0.1 μg/kg · min) on both basal and TRH-stimulated prolactin release in normal and hyperprolactinemic individuals. Sixteen normally menstruating women in the early follicular phase of a cycle and 23 hyperprolactinemic patients were studied. 0.1 μg/kg · min DA was infused in 8 normal women and 15 patients with pathological hyperprolactinemia, while 8 normal controls and 8 patients received 0.02 μg/kg · min DA TRH (200 μg, i-v.) was administered alone and at the 180th min of the 5-hour DA infusion in all controls and patients. A significant reduction in serum PRL levels, which was similar in normal women (-59.5 ± 4.0%, mean ± SE) and hyperprolactinemic patients (-48.2 ± 5.5) was observed in response to 0.1 μg/kg · min DA. In normal cycling women DA infusion significantly (P < 0.02) reduced the PRL response to TRH with respect to the basal TRH test (Δ PRL 45.0 ± 7.0 vs. 77.9 ± 15.4 ng/ml). On the contrary, the PRL response to TRH was significantly higher during 0.1 μg/kg · min DA than in basal conditions in hyperprolactinemic patients, both in absolute (Δ PRL 91.8 ± 17.6 vs. 38.4 ± 6.8, P < 0.03) and per cent (198.5 ± 67.6 vs. 32.1 ± 7.5, P < 0.02) values. A normal PRL response to TRH, arbitrarily defined as an increase > 100% of baseline, was restored in 11 out of 15 previously unresponsive hyperprolactinemic patients. PRL levels decreased by 33.4 ± 5.0% in normal cycling women during 0.02 μg/kg · min DA infusion, but such a DA infusion rate did not affect the PRL response to TRH in this group (Δ PRL 77.7 ± 12.6 in the basal TRH test, 83.2 ± 12.0 during DA). Finally, 0.02 μg/kg · min DA did not induce any significant reduction in PRL serum levels in hyperprolactinemic women (-4.6 ± 3.8% of baseline P < 0.001 vs. normal women) and did not modify the PRL unresponsiveness to TRH (Δ % PRL 38.9 ± 10.1 in basal conditions, 48.8 ± 14.6 during 0.02 μg/kg · min DA). The results demonstrate that PRL unresponsiveness to TRH in pathological hyperprolactinemia is not the expression of an intrinsic adenomatous lactotroph defect, but simply the result of an already overstimulated PRL secretion due to a defective DA inhibition of pituitary lactotrophs. The PRL response to a very low DA infusion rate (0.02 μg/kg · min) was significantly reduced in hyperprolactinemic patients, but the importance of this relative DA resistance in the development and/or maintenance of pathological hyperprolactinemia remains to be elucidated.
    Language English
    Publishing date 1987-03-01
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 80125-2
    ISSN 1439-4286 ; 0018-5043
    ISSN (online) 1439-4286
    ISSN 0018-5043
    DOI 10.1055/s-2007-1011757
    Database Thieme publisher's database

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