Pub Date : 2016-10-01DOI: 10.1097/XCE.0000000000000097
J. Petrie
Adipose tissue in the right quantity, in the right place, at the right time, doing the right thing: that was the message from the recent annual European group for the study of insulin resistance (EGIR) meeting expertly hosted by Andrea Natali in his home town of Pisa, Italy. On the occasion of this 25th meeting, group members welcomed back its founding President Ele Ferrannini (also a native of Pisa) to another term in office after a 15-year interlude.
{"title":"Adipose tissue expansion: impact on insulin sensitivity, β-cell function, liver function and cardiovascular health. European Group for the Study of Insulin Resistance (EGIR) annual scientific meeting; Pisa, Italy; 12–14th May 2016","authors":"J. Petrie","doi":"10.1097/XCE.0000000000000097","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000097","url":null,"abstract":"Adipose tissue in the right quantity, in the right place, at the right time, doing the right thing: that was the message from the recent annual European group for the study of insulin resistance (EGIR) meeting expertly hosted by Andrea Natali in his home town of Pisa, Italy. On the occasion of this 25th meeting, group members welcomed back its founding President Ele Ferrannini (also a native of Pisa) to another term in office after a 15-year interlude.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88100326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000093
M. Christensen, F. Knop
The incretin hormone glucose-dependent insulinotropic polypeptide (GIP) is secreted by enteroendocrine cells in the intestinal mucosa in response to nutrient ingestion. It is well known that GIP exerts a strong, glucose-dependent (during elevated blood glucose levels) insulinotropic effect. In recent years, it has become clear that GIP also exerts effects on glucagon secretion. The regulation of glucagon secretion is interesting as the combination of inadequate insulin secretion and excessive glucagon secretion represents an essential contributor towards the hyperglycaemia in patients with type 2 diabetes. Moreover, the absence of a well-timed counterregulatory glucagon response contributes towards an increased risk of hypoglycaemia in patients with type 1 diabetes. Here, we review several studies investigating the effect of GIP on glucagon secretion and discuss the current evidence for a glucose-dependent glucagonotropic effect of GIP in healthy individuals and in patients with diabetes, respectively. We conclude that at fasting glycaemia and lower levels of glycaemia, GIP seems to increase glucagon secretion, with little effect on insulin release, which points towards a bifunctional blood glucose-stabilizing role of GIP in healthy humans. In patients with type 2 diabetes, GIP may contribute to inappropriate glucagon secretion and in patients with type 1 diabetes, GIP augments glucagon responses to hypoglycaemia.
{"title":"Effects of glucose-dependent insulinotropic polypeptide on glucagon","authors":"M. Christensen, F. Knop","doi":"10.1097/XCE.0000000000000093","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000093","url":null,"abstract":"The incretin hormone glucose-dependent insulinotropic polypeptide (GIP) is secreted by enteroendocrine cells in the intestinal mucosa in response to nutrient ingestion. It is well known that GIP exerts a strong, glucose-dependent (during elevated blood glucose levels) insulinotropic effect. In recent years, it has become clear that GIP also exerts effects on glucagon secretion. The regulation of glucagon secretion is interesting as the combination of inadequate insulin secretion and excessive glucagon secretion represents an essential contributor towards the hyperglycaemia in patients with type 2 diabetes. Moreover, the absence of a well-timed counterregulatory glucagon response contributes towards an increased risk of hypoglycaemia in patients with type 1 diabetes. Here, we review several studies investigating the effect of GIP on glucagon secretion and discuss the current evidence for a glucose-dependent glucagonotropic effect of GIP in healthy individuals and in patients with diabetes, respectively. We conclude that at fasting glycaemia and lower levels of glycaemia, GIP seems to increase glucagon secretion, with little effect on insulin release, which points towards a bifunctional blood glucose-stabilizing role of GIP in healthy humans. In patients with type 2 diabetes, GIP may contribute to inappropriate glucagon secretion and in patients with type 1 diabetes, GIP augments glucagon responses to hypoglycaemia.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"27 1","pages":"75–81"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80235711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000087
C. Hölscher
Type 2 diabetes is a risk factor for developing chronic neurodegenerative disorders such as Alzheimer’s disease (AD) or Parkinson’s disease (PD). The underlying mechanism appears to be insulin desensitization in the brain. A range of glucagon-like peptide 1 (GLP-1) mimetics and glucose-dependent insulinotropic polypeptide (GIP) analogues initially designed to treat diabetes protected transgenic animals that model AD and toxin-based animal models of PD. Novel dual GLP-1/GIP analogues also show good neuroprotective effects. On the basis of these findings, first clinical trials have been conducted. In a pilot study on patients with AD, the GLP-1 analogue liraglutide showed good protective effects in 18F-fluorodeoxyglucose (18F-FDG)-PET brain imaging. It was found that the disease-related decay of brain activity had been completely stopped by the drug. In a pilot study in patients with PD, the GLP-1 mimetic exendin-4 showed good protection from motor and cognitive impairments. These results demonstrate the potential of developing disease-modifying treatments for AD and PD.
{"title":"Glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide analogues as novel treatments for Alzheimer’s and Parkinson’s disease","authors":"C. Hölscher","doi":"10.1097/XCE.0000000000000087","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000087","url":null,"abstract":"Type 2 diabetes is a risk factor for developing chronic neurodegenerative disorders such as Alzheimer’s disease (AD) or Parkinson’s disease (PD). The underlying mechanism appears to be insulin desensitization in the brain. A range of glucagon-like peptide 1 (GLP-1) mimetics and glucose-dependent insulinotropic polypeptide (GIP) analogues initially designed to treat diabetes protected transgenic animals that model AD and toxin-based animal models of PD. Novel dual GLP-1/GIP analogues also show good neuroprotective effects. On the basis of these findings, first clinical trials have been conducted. In a pilot study on patients with AD, the GLP-1 analogue liraglutide showed good protective effects in 18F-fluorodeoxyglucose (18F-FDG)-PET brain imaging. It was found that the disease-related decay of brain activity had been completely stopped by the drug. In a pilot study in patients with PD, the GLP-1 mimetic exendin-4 showed good protection from motor and cognitive impairments. These results demonstrate the potential of developing disease-modifying treatments for AD and PD.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"517 1","pages":"93–98"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77139797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000091
J. Holst
Gut hormone secretion in response to nutrient ingestion appears to depend on membrane proteins expressed by the enteroendocrine cells. These include transporters (glucose and amino acid transporters), and, in this case, hormone secretion depends on metabolic and electrophysiological events elicited by absorption of the nutrient. In other cases (e.g. lipid ingestion and digestion), stimulation may result from interaction with G-protein-coupled receptors expressed by the endocrine cells and activation of intracellular signals (cAMP, IP3, etc.). It is the rate at which these mechanisms are being activated that determines hormone responses. It follows that operations that change intestinal exposure to and absorption of nutrients, such as gastric bypass operations, also change hormone secretion. This results in exaggerated increases in the secretion of particularly the distal small intestinal hormones, GLP-1, GLP-2, oxyntomodulin, neurotensin and peptide YY (PYY). However, some proximal hormones also show changes probably reflecting that the distribution of these hormones is not restricted to the bypassed segments of the gut. Thus, cholecystokinin responses are increased, whereas gastric inhibitory polypeptide responses are relatively unchanged. Increased secretion of cholecystokinin, neurotensin, GLP-1 and PYY may contribute to the appetite inhibitory effect and, therefore, the weight loss after the operations. Indeed, in experiments in which the actions of PYY and GLP-1 were prevented, food intake increased by 20%. The increased insulin responses after the operation, one of the important mechanisms whereby these operations cause diabetes remission, is clearly due to a combination of the increased glucose absorption rates and the exaggerated GLP-1 secretion. The hormonal changes are therefore very important for the metabolic effects of the operations.
{"title":"Gut hormones and gastric bypass","authors":"J. Holst","doi":"10.1097/XCE.0000000000000091","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000091","url":null,"abstract":"Gut hormone secretion in response to nutrient ingestion appears to depend on membrane proteins expressed by the enteroendocrine cells. These include transporters (glucose and amino acid transporters), and, in this case, hormone secretion depends on metabolic and electrophysiological events elicited by absorption of the nutrient. In other cases (e.g. lipid ingestion and digestion), stimulation may result from interaction with G-protein-coupled receptors expressed by the endocrine cells and activation of intracellular signals (cAMP, IP3, etc.). It is the rate at which these mechanisms are being activated that determines hormone responses. It follows that operations that change intestinal exposure to and absorption of nutrients, such as gastric bypass operations, also change hormone secretion. This results in exaggerated increases in the secretion of particularly the distal small intestinal hormones, GLP-1, GLP-2, oxyntomodulin, neurotensin and peptide YY (PYY). However, some proximal hormones also show changes probably reflecting that the distribution of these hormones is not restricted to the bypassed segments of the gut. Thus, cholecystokinin responses are increased, whereas gastric inhibitory polypeptide responses are relatively unchanged. Increased secretion of cholecystokinin, neurotensin, GLP-1 and PYY may contribute to the appetite inhibitory effect and, therefore, the weight loss after the operations. Indeed, in experiments in which the actions of PYY and GLP-1 were prevented, food intake increased by 20%. The increased insulin responses after the operation, one of the important mechanisms whereby these operations cause diabetes remission, is clearly due to a combination of the increased glucose absorption rates and the exaggerated GLP-1 secretion. The hormonal changes are therefore very important for the metabolic effects of the operations.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"27 2","pages":"69–74"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/XCE.0000000000000091","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72373889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000095
J. Rehfeld
This review argues that cholecystokinin (CCK) and gastrin are incretins. The insulin cells are equipped with CCK2/gastrin receptors. CCK/gastrin peptides stimulate insulin secretion and potentiate the incretin effect of glucagon-like peptide-1. CCK/gastrin and insulin are released in significant amounts during normal mixed meals even at modest changes in blood glucose concentrations. Treatment of diabetes patients with combinatorial glucagon-like peptide-1 and CCK or gastrin-derived constructs therefore provides an expedient option.
{"title":"Why cholecystokinin and gastrin are also incretins","authors":"J. Rehfeld","doi":"10.1097/XCE.0000000000000095","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000095","url":null,"abstract":"This review argues that cholecystokinin (CCK) and gastrin are incretins. The insulin cells are equipped with CCK2/gastrin receptors. CCK/gastrin peptides stimulate insulin secretion and potentiate the incretin effect of glucagon-like peptide-1. CCK/gastrin and insulin are released in significant amounts during normal mixed meals even at modest changes in blood glucose concentrations. Treatment of diabetes patients with combinatorial glucagon-like peptide-1 and CCK or gastrin-derived constructs therefore provides an expedient option.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"56 1","pages":"99–101"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90437402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000086
J. Ussher, Jonathan E. Campbell
The gut incretin hormone, glucagon-like peptide 1 (GLP-1), regulates islet hormone secretion, circulating glucose levels, and body weight, making it an attractive agent for the treatment of type 2 diabetes. As cardiovascular disease represents the leading cause of death in patients with diabetes, it is important to understand how GLP-1-based drugs impact the cardiovascular system. Here, we review recent advances in our understanding of two incretin-based drug classes, GLP-1 receptor agonists and dipeptidyl peptidase 4 inhibitors, specifically in the context of heart failure. In addition to illustrating how these therapies influence cardiac signaling processes, we describe the cardioprotective mechanisms identified in preclinical studies, while reviewing the clinical data from studies in patients with type 2 diabetes. We end by speculating why observations made in preclinical studies are not necessarily reflected in a clinically relevant patient population.
{"title":"Incretin-based therapies for the failing heart","authors":"J. Ussher, Jonathan E. Campbell","doi":"10.1097/XCE.0000000000000086","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000086","url":null,"abstract":"The gut incretin hormone, glucagon-like peptide 1 (GLP-1), regulates islet hormone secretion, circulating glucose levels, and body weight, making it an attractive agent for the treatment of type 2 diabetes. As cardiovascular disease represents the leading cause of death in patients with diabetes, it is important to understand how GLP-1-based drugs impact the cardiovascular system. Here, we review recent advances in our understanding of two incretin-based drug classes, GLP-1 receptor agonists and dipeptidyl peptidase 4 inhibitors, specifically in the context of heart failure. In addition to illustrating how these therapies influence cardiac signaling processes, we describe the cardioprotective mechanisms identified in preclinical studies, while reviewing the clinical data from studies in patients with type 2 diabetes. We end by speculating why observations made in preclinical studies are not necessarily reflected in a clinically relevant patient population.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"44 1","pages":"86–92"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75949572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000088
B. Omar, B. Ahrén
Dipeptidyl peptidase 4 (DPP-4) inhibitors are now being clinically utilized as glucose-lowering medications for the treatment of type 2 diabetes. Their widespread use and effective glucose-lowering properties have led to great interest in the mechanism of action of this class of drug. Although it has been well accepted that DPP-4 inhibitors lower glucose in part by increasing postprandial insulin secretion and suppressing fasting and postprandial hyperglucagonemia, recent studies have suggested that DPP-4 inhibition has other metabolically beneficial properties that are extrapancreatic in nature. This review explores the changes in DPP-4 expression and activity in metabolic disease states and discusses the metabolic consequences of DPP-4 inhibition on a systemic and tissue-specific basis. It concludes that there is considerable scientific evidence and a growing body of clinical evidence to suggest that DPP-4 inhibition would be beneficial in a number of metabolic disorders in addition to type 2 diabetes.
{"title":"Extrapancreatic contribution to glucose regulation by dipeptidyl peptidase 4 inhibition","authors":"B. Omar, B. Ahrén","doi":"10.1097/XCE.0000000000000088","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000088","url":null,"abstract":"Dipeptidyl peptidase 4 (DPP-4) inhibitors are now being clinically utilized as glucose-lowering medications for the treatment of type 2 diabetes. Their widespread use and effective glucose-lowering properties have led to great interest in the mechanism of action of this class of drug. Although it has been well accepted that DPP-4 inhibitors lower glucose in part by increasing postprandial insulin secretion and suppressing fasting and postprandial hyperglucagonemia, recent studies have suggested that DPP-4 inhibition has other metabolically beneficial properties that are extrapancreatic in nature. This review explores the changes in DPP-4 expression and activity in metabolic disease states and discusses the metabolic consequences of DPP-4 inhibition on a systemic and tissue-specific basis. It concludes that there is considerable scientific evidence and a growing body of clinical evidence to suggest that DPP-4 inhibition would be beneficial in a number of metabolic disorders in addition to type 2 diabetes.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"13 3 1","pages":"82–85"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78480565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000092
D. Sonne
The incretin effect refers to the enhanced insulin secretion in response to oral or enteric glucose. More specifically, the incretin effect designates the augmentation of insulin secretion after oral administration of glucose compared with insulin secretion levels observed after intravenous glucose administered to mimic the plasma glucose excursion elicited by the oral load [1–4]. The incretin effect is due to hormones secreted from the intestine, the most important ones being glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Both these hormones stimulate pancreatic insulin secretion. GLP-1, in addition, exerts suppressive effects on pancreatic glucagon secretion, gastrointestinal motility, appetite, and food intake [5]. GIP, however, exerts both glucagonotropic (during conditions with low plasma glucose) and glucagon-neutral (during conditions with high plasma glucose) effects [6]. Both GLP-1 and GIP are metabolized rapidly by the ubiquitous enzyme dipeptidyl peptidase 4 (DPP-4), which truncates the N-terminal ends, whereby the biological activity of both hormones as for insulin secretion is abolished [5].
{"title":"Glucometabolic gut hormones: beyond the incretin effect","authors":"D. Sonne","doi":"10.1097/XCE.0000000000000092","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000092","url":null,"abstract":"The incretin effect refers to the enhanced insulin secretion in response to oral or enteric glucose. More specifically, the incretin effect designates the augmentation of insulin secretion after oral administration of glucose compared with insulin secretion levels observed after intravenous glucose administered to mimic the plasma glucose excursion elicited by the oral load [1–4]. The incretin effect is due to hormones secreted from the intestine, the most important ones being glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Both these hormones stimulate pancreatic insulin secretion. GLP-1, in addition, exerts suppressive effects on pancreatic glucagon secretion, gastrointestinal motility, appetite, and food intake [5]. GIP, however, exerts both glucagonotropic (during conditions with low plasma glucose) and glucagon-neutral (during conditions with high plasma glucose) effects [6]. Both GLP-1 and GIP are metabolized rapidly by the ubiquitous enzyme dipeptidyl peptidase 4 (DPP-4), which truncates the N-terminal ends, whereby the biological activity of both hormones as for insulin secretion is abolished [5].","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"5 1","pages":"68"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83197063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000084
J. Hansen, P. Plomgaard
Fibroblast growth factor 21 (FGF21) is a novel metabolic regulator that holds promise as a therapeutic target in the treatment of type 2 diabetes and obesity. The regulation of FGF21, however, is only emerging. Most of the existing evidence is derived from animal studies – particularly mice – where repeated measurements of hormones are difficult. Over the last decade, several studies evaluating the regulation of FGF21 in human physiology have emerged in the literature. These have shown that plasma FGF21 is an acutely regulated hormone and that the glucagon-to-insulin ratio seems to be pivotal in the regulation of FGF21. In the present narrative review, we evaluate the regulation of FGF21 in humans with a focus on the regulatory role of the glucagon-to-insulin ratio.
{"title":"Fibroblast growth factor 21: new insights from human studies","authors":"J. Hansen, P. Plomgaard","doi":"10.1097/XCE.0000000000000084","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000084","url":null,"abstract":"Fibroblast growth factor 21 (FGF21) is a novel metabolic regulator that holds promise as a therapeutic target in the treatment of type 2 diabetes and obesity. The regulation of FGF21, however, is only emerging. Most of the existing evidence is derived from animal studies – particularly mice – where repeated measurements of hormones are difficult. Over the last decade, several studies evaluating the regulation of FGF21 in human physiology have emerged in the literature. These have shown that plasma FGF21 is an acutely regulated hormone and that the glucagon-to-insulin ratio seems to be pivotal in the regulation of FGF21. In the present narrative review, we evaluate the regulation of FGF21 in humans with a focus on the regulatory role of the glucagon-to-insulin ratio.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"56 1","pages":"112–116"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78441925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-09-01DOI: 10.1097/XCE.0000000000000085
C. Ratner, C. Hundahl, B. Holst
Neurotensin (NT) is a 13 amino acid peptide hormone primarily expressed in the brain and in the gastrointestinal (GI) tract. NT in the brain is generally considered an anorexigenic neuropeptide, but the potential metabolic actions of GI tract NT have not been investigated extensively. In the GI tract, NT is mainly found in so-called N cells, but is also coexpressed with a number of functionally related hormones including glucagon-like peptide-1 (GLP-1) and peptide YY. NT, GLP-1, and peptide YY can further be released together in response to a number of different physiological stimuli and can coact on some but not all target organs. In line with the recent focus on developing antiobesity agents targeting more than one signaling pathway, NT may be a candidate for such polytherapy drugs in combination with other gut hormones such as GLP-1.
{"title":"The metabolic actions of neurotensin secreted from the gut","authors":"C. Ratner, C. Hundahl, B. Holst","doi":"10.1097/XCE.0000000000000085","DOIUrl":"https://doi.org/10.1097/XCE.0000000000000085","url":null,"abstract":"Neurotensin (NT) is a 13 amino acid peptide hormone primarily expressed in the brain and in the gastrointestinal (GI) tract. NT in the brain is generally considered an anorexigenic neuropeptide, but the potential metabolic actions of GI tract NT have not been investigated extensively. In the GI tract, NT is mainly found in so-called N cells, but is also coexpressed with a number of functionally related hormones including glucagon-like peptide-1 (GLP-1) and peptide YY. NT, GLP-1, and peptide YY can further be released together in response to a number of different physiological stimuli and can coact on some but not all target organs. In line with the recent focus on developing antiobesity agents targeting more than one signaling pathway, NT may be a candidate for such polytherapy drugs in combination with other gut hormones such as GLP-1.","PeriodicalId":72529,"journal":{"name":"Cardiovascular endocrinology","volume":"31 1","pages":"102–111"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79299672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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