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Jens J. Holst - One of the best experts on this subject based on the ideXlab platform.

  • pancreatic polypeptide a potential biomarker of gip receptor activation in vivo
    Diabetic Medicine, 2021
    Co-Authors: Simon Veedfald, Jens J. Holst, Tina Vilsboll, Natasha C Bergmann, Mikkel B Christensen, Filip K Knop
    Abstract:

    The Insulinotropic gut hormones glucose-dependent Insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are key factors in the regulation of normal postprandial glucose homeostasis, but in most reports, the glucose-lowering effect of GIP has been shown to be blunted or even absent in people with type 2 diabetes (T2D) (1). Despite previous reports that GIP does not potentiate the glucose-lowering effect of GLP-1 in type 2 diabetes (2), a dual GIP/GLP-1 receptor agonist (tirzepatide/LY3298176) has recently been reported to reduce HbA1c and body weight in overweight/obese individuals with type 2 diabetes beyond that of GLP-1 receptor monoagonism (dulaglutide) (3).

  • postprandial levels of glp 1 gip and glucagon after 2 years of weight loss with a paleolithic diet a randomised controlled trial in healthy obese women
    European Journal of Endocrinology, 2019
    Co-Authors: Julia Otten, Jens J. Holst, Mats Ryberg, Caroline Mellberg, Bernt Lindahl, Christel Larsson, Elin Chorell, Tomas Andersson, Tommy Olsson
    Abstract:

    OBJECTIVE: To investigate how weight loss by different diets impacts on postprandial levels of glucagon-like peptide 1 (GLP-1), glucose-dependent Insulinotropic polypeptide (GIP), and glucagon.METH ...

  • glucose dependent Insulinotropic polypeptide promotes lipid deposition in subcutaneous adipocytes in obese type 2 diabetes patients a maladaptive response
    American Journal of Physiology-endocrinology and Metabolism, 2017
    Co-Authors: Sravan Thondam, Jens J. Holst, Christina Daousi, John P H Wilding, Gulizar Issa Ameen, Chenjing Yang, Catherine Whitmore, Silvia Mora, Daniel J Cuthbertson
    Abstract:

    Glucose-dependent Insulinotropic polypeptide (GIP) beyond its Insulinotropic effects may regulate postprandial lipid metabolism. Whereas the Insulinotropic action of GIP is known to be impaired in type 2 diabetes mellitus (T2DM), its adipogenic effect is unknown. We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Twenty-three subjects categorized into four groups, normoglycemic lean (n = 6), normoglycemic obese (n = 6), obese with impaired glucose regulation (IGR; n = 6), and obese T2DM (n = 5), participated in a double-blind, randomized, crossover study involving a hyperglycemic clamp with a 240-min GIP infusion (2 pmol·kg-1·min-1) or normal saline. Insulin, NEFA, SAT-TAG content, and gene expression of key lipogenic enzymes were determined before and immediately after GIP/saline infusions. GIP lowered NEFA concentrations in the obese T2DM group despite diminished Insulinotropic activity (mean NEFA AUC0-4 h ± SE, 41,992 ± 9,843 µmol·l-1·min-1 vs. 71,468 ± 13,605 with placebo, P = 0.039, 95% CI: 0.31-0.95). Additionally, GIP increased SAT-TAG in obese T2DM (1.78 ± 0.4 vs 0.86 ± 0.1-fold with placebo, P = 0.043, 95% CI: 0.1-1.8). Such effect with GIP was not observed in other three groups despite greater Insulinotropic activity. Reduction in NEFA concentration with GIP correlated with adipose tissue insulin resistance for all subjects (Pearson, r = 0.56, P = 0.005). There were no significant gene expression changes in key SAT lipid metabolism enzymes. In conclusion, GIP appears to promote fat accretion and thus may exacerbate obesity and insulin resistance in T2DM.

  • the role of efferent cholinergic transmission for the Insulinotropic and glucagonostatic effects of glp 1
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Astrid Plamboeck, Tina Vilsboll, Filip K Knop, Simon Veedfald, Carolyn F. Deacon, Bolette Hartmann, Jens J. Holst
    Abstract:

    The importance of vagal efferent signaling for the Insulinotropic and glucagonostatic effects of glucagon-like peptide-1 (GLP-1) was investigated in a randomized single-blinded study. Healthy male ...

  • restoration of the Insulinotropic effect of glucose dependent Insulinotropic polypeptide contributes to the antidiabetic effect of dipeptidyl peptidase 4 inhibitors
    Diabetes Obesity and Metabolism, 2015
    Co-Authors: Kasper Aaboe, Jens J. Holst, Sten Madsbad, Carolyn F. Deacon, S Akram, Thure Krarup
    Abstract:

    Aims To examine whether 12 weeks of treatment with a dipeptidyl peptidase-4 (DPP-4) inhibitor, sitagliptin, influences the insulin secretion induced by glucose, glucose-dependent Insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) during a hyperglycaemic clamp in patients with type 2 diabetes (T2DM). Methods A randomized, double-blind, placebo-controlled study was conducted over 12 weeks, during which 25 patients with T2DM completed treatment with either sitagliptin (100 mg once daily) or placebo as add-on therapy to metformin [sitagliptin group (n = 12): mean ± standard error of the mean (s.e.m.) age 54 ± 2.5 years, mean ± s.e.m. HbA1c 7.8 ± 0.2%; placebo group (n = 13): mean ± s.e.m. age: 57 ± 3.0 years, mean ± s.e.m. HbA1c 7.9 ± 0.2 %]. In weeks 1 and 12, the patients underwent three 2-h 15-mM hyperglycaemic clamp experiments with infusion of either saline, GLP-1 or GIP. β-cell function was evaluated according to first-phase, second-phase, incremental and total insulin and C-peptide responses. Results In the sitagliptin group, the mean HbA1c concentration was significantly reduced by 0.9% (p = 0.01). The total β-cell response during GIP infusion improved signficantly from week 1 to week 12, both within the sitagliptin group (p = 0.004) and when compared with the placebo group (p = 0.04). The total β-cell response during GLP-1 infusion was significantly higher (p = 0.001) when compared with saline and GIP infusion, but with no improvement from week 1 to week 12. No significant changes in β-cell function occurred in the placebo group. Conclusions Treatment with the DPP-4 inhibitor sitagliptin over 12 weeks in patients with T2DM partially restored the lost Insulinotropic effect of GIP, whereas the preserved Insulinotropic effect of GLP-1 was not further improved. A gradual enhancement of the Insulinotropic effect of GIP, therefore, possibly contributes to the antidiabetic actions of DPP-4 inhibitors.

Michael A. Nauck - One of the best experts on this subject based on the ideXlab platform.

  • no evidence of tachyphylaxis for Insulinotropic actions of glucose dependent Insulinotropic polypeptide gip in subjects with type 2 diabetes their first degree relatives or in healthy subjects
    Peptides, 2020
    Co-Authors: Michael A. Nauck, J J Holst, Carolyn F. Deacon, H Holle, Melanie Kahle, A Tytko, Juris J Meier
    Abstract:

    Abstract Background, aims In patients with type 2 diabetes, the lost Insulinotropic effect of the incretin hormone glucose-dependent Insulinotropic polypeptide (GIP) is more apparent after continuous versus bolus administration. To test whether the difference might be explained by rapid tachyphylaxis in response to elevated concentrations of GIP, and whether patients with type 2 diabetes and their relatives are more susceptible to tachyphylaxis than healthy subjects. Patients and Methods In a two-way crossover design, Insulinotropic responses to repeated bolus injection (50 pmol/kg body weight at 30 and 120 min) and continuous infusion of GIP (2 pmol.kg-1.min-1 from 30 to 180 min) under hyperglycaemic clamp conditions (8.5 mmol/l) was compared in age- gender- and weight-matched patients with type 2 diabetes, first degree relatives of such patients, and healthy subjects. Results Insulin secretory responses to the first and second GIP bolus were not significantly different in any of the subject groups. Subjects with type 2 diabetes had a significant relative impairment versus healthy subjects with continuous (C-peptide, −13.2 %, p  Conclusions Rapid tachyphylaxis in response to continuous exposure to slightly supraphysiological concentrations of GIP does not explain the reduced Insulinotropic response to GIP infusions in patients with type 2 diabetes or their first-degree relatives.

  • gip does not potentiate the antidiabetic effects of glp 1 in hyperglycemic patients with type 2 diabetes
    Diabetes, 2011
    Co-Authors: Nikolaos Mentis, Jens J. Holst, Carolyn F. Deacon, Michael J. Theodorakis, Juris J Meier, Irfan Vardarli, Lars D Kothe, Michael A. Nauck
    Abstract:

    OBJECTIVE The incretin glucagon-like peptide 1 (GLP-1) exerts Insulinotropic activity in type 2 diabetic patients, whereas glucose-dependent Insulinotropic polypeptide (GIP) no longer does. We studied whether GIP can alter the Insulinotropic or glucagonostatic activity of GLP-1 in type 2 diabetic patients. RESEARCH DESIGN AND METHODS Twelve patients with type 2 diabetes (nine men and three women; 61 ± 10 years; BMI 30.0 ± 3.7 kg/m 2 ; HbA 1c 7.3 ± 1.5%) were studied. In randomized order, intravenous infusions of GLP-1(7-36)-amide (1.2 pmol · kg −1 · min −1 ), GIP (4 pmol · kg −1 · min −1 ), GLP-1 plus GIP, and placebo were administered over 360 min after an overnight fast (≥1 day wash-out period between experiments). Capillary blood glucose, plasma insulin, C-peptide, glucagon, GIP, GLP-1, and free fatty acids (FFA) were determined. RESULTS Exogenous GLP-1 alone reduced glycemia from 10.3 to 5.1 ± 0.2 mmol/L. Insulin secretion was stimulated (insulin, C-peptide, P P = 0.009). With GIP alone, glucose was lowered slightly ( P = 0.0021); insulin and C-peptide were stimulated to a lesser degree than with GLP-1 ( P P = 0.90; C-peptide, P = 0.85). Rather, the suppression of glucagon elicited by GLP-1 was antagonized by the addition of GIP ( P = 0.008). FFA were suppressed by GLP-1 ( P P = 0.07). CONCLUSIONS GIP is unable to further amplify the Insulinotropic and glucose-lowering effects of GLP-1 in type 2 diabetes. Rather, the suppression of glucagon by GLP-1 is antagonized by GIP.

  • impact of exogenous hyperglucagonemia on postprandial concentrations of gastric inhibitory polypeptide and glucagon like peptide 1 in humans
    The Journal of Clinical Endocrinology and Metabolism, 2010
    Co-Authors: Juris J Meier, W E Schmidt, Carolyn F. Deacon, Peter R Ritter, Alexandra Jacob, Bjoern A Menge, Michael A. Nauck
    Abstract:

    Background: Postprandial secretion of glucagon-like peptide 1 (GLP-1) has been found diminished in some patients with type 2 diabetes mellitus (T2DM) and high glucagon concentrations. We examined the effects of exogenous glucagon on the release of incretin hormones. Patients and Methods: Ten patients with T2DM and 10 healthy controls were examined with a meal test during the iv administration of glucagon 0.65 ng/kg · min and placebo. Results: GLP-1 plasma concentration increased after meal ingestion in both groups (P < 0.0001), but postprandial GLP-1 plasma levels were not affected by glucagon administration. However, immediately after cessation of the glucagon infusion, GLP-1 levels increased by about 2-fold to levels of 51.8 ± 14.6 pmol/liter in the T2DM patients and 58.9 ± 20.0 pmol/liter in controls (P < 0.05). The time courses of glucose-dependent Insulinotropic peptide glucose-dependent Insulinotropic peptide and GLP-1 concentrations were not different between T2DM patients and controls during the p...

  • is the diminished incretin effect in type 2 diabetes just an epi phenomenon of impaired β cell function
    Diabetes, 2010
    Co-Authors: Juris J Meier, Michael A. Nauck
    Abstract:

    Type 2 diabetes is characterized by a deficit in β-cell mass, impaired insulin secretion in response to various stimuli (1–3), as well as a variable extent of insulin resistance (4). More specifically, regarding β-cell function, a significant reduction of the incretin effect, i.e., the postprandial augmentation of insulin secretion by gut hormones, has been described in patients with type 2 diabetes (5). Thus, while the two incretin hormones gastric inhibitory polypeptide (glucose-dependent insulinotopic polypeptide [GIP]) and glucagon-like peptide 1 (GLP-1) are held responsible for ∼50–70% of the postprandial insulin responses in healthy individuals (6), their contribution to the overall insulin responses after oral glucose ingestion may amount to <20% in patients with type 2 diabetes (5,7). The reasons underlying the loss of incretin activity in type 2 diabetes are still incompletely understood. The present article reviews the available evidence regarding disturbances in the enteroinsular axis in patients with type 2 diabetes and provides possible explanations for their etiologies, focusing on the personal experience of the authors. ### Secretion of incretin hormones in patients with type 2 diabetes. Because the incretin effect has been related to the secretion and Insulinotropic action of GIP and GLP-1 (8,9), it was obvious to compare these parameters between patients with type 2 diabetes and healthy control subjects: Regarding the secretion of GIP, elevated, normal, and reduced plasma levels have been described in patients with type 2 diabetes (10–15). However, taking together all the evidence available, the secretion of GIP appears to be relatively unchanged in type 2 diabetic patients. For GLP-1 release, the case is even more complex. Several studies have reported significant reductions in GLP-1 levels after mixed meal ingestion in patients with type 2 diabetes (10,16,17). In addition, one study has found minor impairments in GLP-1 levels in individuals with impaired glucose …

  • gastric inhibitory polypeptide and glucagon like peptide 1 in the pathogenesis of type 2 diabetes
    Diabetes, 2004
    Co-Authors: Michael A. Nauck, Birgit Baller, Juris J Meier
    Abstract:

    The incretin effect denominates the phenomenon that oral glucose elicits a higher insulin response than does intravenous glucose. The two hormones responsible for the incretin effect, glucose-dependent Insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. In patients with type 2 diabetes, the incretin effect is reduced, and there is a moderate degree of GLP-1 hyposecretion. However, the Insulinotropic response to GLP-1 is well maintained in type 2 diabetes. GIP is secreted normally or hypersecreted in type 2 diabetes; however, the responsiveness of the endocrine pancreas to GIP is greatly reduced. In ∼50% of first-degree relatives of patients with type 2 diabetes, similarly reduced Insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. This opens the possibility that a reduced responsiveness to GIP is an early step in the pathogenesis of type 2 diabetes. On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes.

Juris J Meier - One of the best experts on this subject based on the ideXlab platform.

  • no evidence of tachyphylaxis for Insulinotropic actions of glucose dependent Insulinotropic polypeptide gip in subjects with type 2 diabetes their first degree relatives or in healthy subjects
    Peptides, 2020
    Co-Authors: Michael A. Nauck, J J Holst, Carolyn F. Deacon, H Holle, Melanie Kahle, A Tytko, Juris J Meier
    Abstract:

    Abstract Background, aims In patients with type 2 diabetes, the lost Insulinotropic effect of the incretin hormone glucose-dependent Insulinotropic polypeptide (GIP) is more apparent after continuous versus bolus administration. To test whether the difference might be explained by rapid tachyphylaxis in response to elevated concentrations of GIP, and whether patients with type 2 diabetes and their relatives are more susceptible to tachyphylaxis than healthy subjects. Patients and Methods In a two-way crossover design, Insulinotropic responses to repeated bolus injection (50 pmol/kg body weight at 30 and 120 min) and continuous infusion of GIP (2 pmol.kg-1.min-1 from 30 to 180 min) under hyperglycaemic clamp conditions (8.5 mmol/l) was compared in age- gender- and weight-matched patients with type 2 diabetes, first degree relatives of such patients, and healthy subjects. Results Insulin secretory responses to the first and second GIP bolus were not significantly different in any of the subject groups. Subjects with type 2 diabetes had a significant relative impairment versus healthy subjects with continuous (C-peptide, −13.2 %, p  Conclusions Rapid tachyphylaxis in response to continuous exposure to slightly supraphysiological concentrations of GIP does not explain the reduced Insulinotropic response to GIP infusions in patients with type 2 diabetes or their first-degree relatives.

  • gip does not potentiate the antidiabetic effects of glp 1 in hyperglycemic patients with type 2 diabetes
    Diabetes, 2011
    Co-Authors: Nikolaos Mentis, Jens J. Holst, Carolyn F. Deacon, Michael J. Theodorakis, Juris J Meier, Irfan Vardarli, Lars D Kothe, Michael A. Nauck
    Abstract:

    OBJECTIVE The incretin glucagon-like peptide 1 (GLP-1) exerts Insulinotropic activity in type 2 diabetic patients, whereas glucose-dependent Insulinotropic polypeptide (GIP) no longer does. We studied whether GIP can alter the Insulinotropic or glucagonostatic activity of GLP-1 in type 2 diabetic patients. RESEARCH DESIGN AND METHODS Twelve patients with type 2 diabetes (nine men and three women; 61 ± 10 years; BMI 30.0 ± 3.7 kg/m 2 ; HbA 1c 7.3 ± 1.5%) were studied. In randomized order, intravenous infusions of GLP-1(7-36)-amide (1.2 pmol · kg −1 · min −1 ), GIP (4 pmol · kg −1 · min −1 ), GLP-1 plus GIP, and placebo were administered over 360 min after an overnight fast (≥1 day wash-out period between experiments). Capillary blood glucose, plasma insulin, C-peptide, glucagon, GIP, GLP-1, and free fatty acids (FFA) were determined. RESULTS Exogenous GLP-1 alone reduced glycemia from 10.3 to 5.1 ± 0.2 mmol/L. Insulin secretion was stimulated (insulin, C-peptide, P P = 0.009). With GIP alone, glucose was lowered slightly ( P = 0.0021); insulin and C-peptide were stimulated to a lesser degree than with GLP-1 ( P P = 0.90; C-peptide, P = 0.85). Rather, the suppression of glucagon elicited by GLP-1 was antagonized by the addition of GIP ( P = 0.008). FFA were suppressed by GLP-1 ( P P = 0.07). CONCLUSIONS GIP is unable to further amplify the Insulinotropic and glucose-lowering effects of GLP-1 in type 2 diabetes. Rather, the suppression of glucagon by GLP-1 is antagonized by GIP.

  • impact of exogenous hyperglucagonemia on postprandial concentrations of gastric inhibitory polypeptide and glucagon like peptide 1 in humans
    The Journal of Clinical Endocrinology and Metabolism, 2010
    Co-Authors: Juris J Meier, W E Schmidt, Carolyn F. Deacon, Peter R Ritter, Alexandra Jacob, Bjoern A Menge, Michael A. Nauck
    Abstract:

    Background: Postprandial secretion of glucagon-like peptide 1 (GLP-1) has been found diminished in some patients with type 2 diabetes mellitus (T2DM) and high glucagon concentrations. We examined the effects of exogenous glucagon on the release of incretin hormones. Patients and Methods: Ten patients with T2DM and 10 healthy controls were examined with a meal test during the iv administration of glucagon 0.65 ng/kg · min and placebo. Results: GLP-1 plasma concentration increased after meal ingestion in both groups (P < 0.0001), but postprandial GLP-1 plasma levels were not affected by glucagon administration. However, immediately after cessation of the glucagon infusion, GLP-1 levels increased by about 2-fold to levels of 51.8 ± 14.6 pmol/liter in the T2DM patients and 58.9 ± 20.0 pmol/liter in controls (P < 0.05). The time courses of glucose-dependent Insulinotropic peptide glucose-dependent Insulinotropic peptide and GLP-1 concentrations were not different between T2DM patients and controls during the p...

  • is the diminished incretin effect in type 2 diabetes just an epi phenomenon of impaired β cell function
    Diabetes, 2010
    Co-Authors: Juris J Meier, Michael A. Nauck
    Abstract:

    Type 2 diabetes is characterized by a deficit in β-cell mass, impaired insulin secretion in response to various stimuli (1–3), as well as a variable extent of insulin resistance (4). More specifically, regarding β-cell function, a significant reduction of the incretin effect, i.e., the postprandial augmentation of insulin secretion by gut hormones, has been described in patients with type 2 diabetes (5). Thus, while the two incretin hormones gastric inhibitory polypeptide (glucose-dependent insulinotopic polypeptide [GIP]) and glucagon-like peptide 1 (GLP-1) are held responsible for ∼50–70% of the postprandial insulin responses in healthy individuals (6), their contribution to the overall insulin responses after oral glucose ingestion may amount to <20% in patients with type 2 diabetes (5,7). The reasons underlying the loss of incretin activity in type 2 diabetes are still incompletely understood. The present article reviews the available evidence regarding disturbances in the enteroinsular axis in patients with type 2 diabetes and provides possible explanations for their etiologies, focusing on the personal experience of the authors. ### Secretion of incretin hormones in patients with type 2 diabetes. Because the incretin effect has been related to the secretion and Insulinotropic action of GIP and GLP-1 (8,9), it was obvious to compare these parameters between patients with type 2 diabetes and healthy control subjects: Regarding the secretion of GIP, elevated, normal, and reduced plasma levels have been described in patients with type 2 diabetes (10–15). However, taking together all the evidence available, the secretion of GIP appears to be relatively unchanged in type 2 diabetic patients. For GLP-1 release, the case is even more complex. Several studies have reported significant reductions in GLP-1 levels after mixed meal ingestion in patients with type 2 diabetes (10,16,17). In addition, one study has found minor impairments in GLP-1 levels in individuals with impaired glucose …

  • gastric inhibitory polypeptide and glucagon like peptide 1 in the pathogenesis of type 2 diabetes
    Diabetes, 2004
    Co-Authors: Michael A. Nauck, Birgit Baller, Juris J Meier
    Abstract:

    The incretin effect denominates the phenomenon that oral glucose elicits a higher insulin response than does intravenous glucose. The two hormones responsible for the incretin effect, glucose-dependent Insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. In patients with type 2 diabetes, the incretin effect is reduced, and there is a moderate degree of GLP-1 hyposecretion. However, the Insulinotropic response to GLP-1 is well maintained in type 2 diabetes. GIP is secreted normally or hypersecreted in type 2 diabetes; however, the responsiveness of the endocrine pancreas to GIP is greatly reduced. In ∼50% of first-degree relatives of patients with type 2 diabetes, similarly reduced Insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. This opens the possibility that a reduced responsiveness to GIP is an early step in the pathogenesis of type 2 diabetes. On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes.

Filip K Knop - One of the best experts on this subject based on the ideXlab platform.

  • pancreatic polypeptide a potential biomarker of gip receptor activation in vivo
    Diabetic Medicine, 2021
    Co-Authors: Simon Veedfald, Jens J. Holst, Tina Vilsboll, Natasha C Bergmann, Mikkel B Christensen, Filip K Knop
    Abstract:

    The Insulinotropic gut hormones glucose-dependent Insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are key factors in the regulation of normal postprandial glucose homeostasis, but in most reports, the glucose-lowering effect of GIP has been shown to be blunted or even absent in people with type 2 diabetes (T2D) (1). Despite previous reports that GIP does not potentiate the glucose-lowering effect of GLP-1 in type 2 diabetes (2), a dual GIP/GLP-1 receptor agonist (tirzepatide/LY3298176) has recently been reported to reduce HbA1c and body weight in overweight/obese individuals with type 2 diabetes beyond that of GLP-1 receptor monoagonism (dulaglutide) (3).

  • gip s involvement in the pathophysiology of type 2 diabetes
    Peptides, 2020
    Co-Authors: Mikkel B Christensen, Tina Vilsboll, Laerke S Gasbjerg, Sebastian M Heimburger, Signe Stensen, Filip K Knop
    Abstract:

    During the past four decades derangements in glucose-dependent Insulinotropic polypeptide (GIP) biology has been viewed upon as contributing factors to various parts of the pathophysiology type 2 diabetes. This overview outlines and discusses the impaired insulin responses to GIP as well as the effect of GIP on glucagon secretion and the potential involvement of GIP in the obesity and bone disease associated with type 2 diabetes. As outlined in this review, it is unlikely that the impaired Insulinotropic effect of GIP occurs as a primary event in the development of type 2 diabetes, but rather develops once the diabetic state is present and beta cells are unable to maintain normoglycemia. In various models, GIP has effects on glucagon secretion, bone and lipid homeostasis, but whether these effects contribute substantially to the pathophysiology of type 2 diabetes is at present controversial. The review also discusses the substantial uncertainty surrounding the translation of preclinical data relating to the GIP system and outline future research directions.

  • A sandwich ELISA for measurement of the primary glucagon-like peptide-1 metabolite.
    American journal of physiology. Endocrinology and metabolism, 2017
    Co-Authors: Nicolai J. Wewer Albrechtsen, Ali Asmar, Frederik Jensen, Signe Toräng, Lene Simonsen, Rune E. Kuhre, Meena Asmar, Simon Veedfald, Astrid Plamboeck, Filip K Knop
    Abstract:

    Glucagon-like peptide-1 (GLP-1) is an incretin hormone secreted from the gastrointestinal tract. It is best known for its glucose-dependent Insulinotropic effects. GLP-1 is secreted in its intact (...

  • the role of efferent cholinergic transmission for the Insulinotropic and glucagonostatic effects of glp 1
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2015
    Co-Authors: Astrid Plamboeck, Tina Vilsboll, Filip K Knop, Simon Veedfald, Carolyn F. Deacon, Bolette Hartmann, Jens J. Holst
    Abstract:

    The importance of vagal efferent signaling for the Insulinotropic and glucagonostatic effects of glucagon-like peptide-1 (GLP-1) was investigated in a randomized single-blinded study. Healthy male ...

  • Unprecedented high insulin secretion in a healthy human subject after intravenous glucagon-like peptide-1: a case report
    BMC research notes, 2014
    Co-Authors: Filip K Knop, Sten Madsbad, Thure Krarup, Asger Lund, Tina Vilsboll
    Abstract:

    Background The gut-derived incretin hormones, glucose-dependent Insulinotropic polypeptide and glucagon-like peptide-1, are released in response to ingestion of nutrients. Both hormones are highly Insulinotropic in strictly glucose-dependent fashions and glucagon-like peptide-1 is often referred to as one of the most Insulinotropic substances known.

Tina Vilsboll - One of the best experts on this subject based on the ideXlab platform.