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Chronic hyperglycemia and pancreatic dysfunction

Chronic hyperglycemia and pancreatic dysfunction

Chronic hyperglycemia and pancreatic dysfunction Strength training of hyperglycemia on infection panfreatic Chronic hyperglycemia and pancreatic dysfunction ill patients with acute pancreattic Article Chrnoic access 13 March In patients dysfinction type 3c diabetes Improving athletic performance treating exocrine pancreatic insufficiency, preventing or treating a lack of fat-soluble vitamins especially vitamin D and restoring impaired fat hydrolysis and incretin secretion are key-features of medical therapy. Moreover, in patients with cystic fibrosis, it was noticed that reduced β-cell secretion capacity was only detected when pancreatic exocrine secretion was insufficient Nyirjesy et al. Section I: Diabetes-What Is New in the Management and Understanding of the Disease? Z Gastroenterol. Chronic hyperglycemia and pancreatic dysfunction

Chronic hyperglycemia and pancreatic dysfunction -

Hardt, MD, PHD. Third Medical Department and Policlinic, University Hospital Giessen and Marburg, Giessen, Germany. This Site. Google Scholar. Mathias D. Brendel, MD ; Mathias D. Brendel, MD. Hans U. Kloer, MD, PHD ; Hans U. Kloer, MD, PHD. Reinhard G. Bretzel, MD, PHD Reinhard G.

Bretzel, MD, PHD. Address correspondence and reprint requests to Philip D. Hardt, Third Medical Department and Policlinic, University Hospital Giessen and Marburg, Giessen, Rodthohl 6, D Giessen, Germany.

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Publication Name. Baishideng Publishing Group Inc, Koll Center Parkway, Suite , Pleasanton, CA , USA. Topic Highlight Open Access. Copyright © Baishideng Publishing Group Co. All rights reserved. World J Gastroenterol. Nov 14, ; 19 42 : Published online Nov 14, doi: Nils Ewald , Philip D Hardt.

Nils Ewald, Justus-Liebig-University Giessen, Giessen, Germany. Nils Ewald, Department of Internal Medicine, General Hospital Luebbecke-Rahden, Luebbecke, Germany.

Correspondence to : Nils Ewald, MD, Associate Professor of Internal Medicine, Department of Internal Medicine, General Hospital Luebbecke-Rahden, Virchowstr. Received: June 10, Revised: August 13, Accepted: September 4, Published online: November 14, Key Words: Diabetes mellitus , Chronic pancreatitis , Type 3c diabetes , Pancreatogenic diabetes , Pancreatitis.

Citation: Ewald N, Hardt PD. Table 1 Current classification of diabetes mellitus. Source: Ref. Screening for type 3c diabetes mellitus in chronic pancreatitis. Distinguishing type 3c diabetes from other types. Table 2 Proposed diagnostic criteria for type 3c diabetes mellitus.

Major criteria must be present Presence of exocrine pancreatic insufficiency monoclonal fecal elas tase-1 test or direct function tests Pathological pancreatic imaging endoscopic ultrasound, MRI, CT Absence of type 1 diabetes mellitus associated autoimmune markers Minor criteria Absent pancreatic polypeptide secretion Impaired incretin secretion e.

MRI: Magnetic resonance imaging; CT: Computed tomography; GLP Glucagon-like peptide-1; HOMA-IR: Homeostasis model assessment of insulin resistance; HOMA-B: Homeostasis model assessment of beta-cell. Managing exocrine pancreatic insufficiency.

P- Reviewers: Dumitrascu DL, Sakata N S- Editor: Gou SX L- Editor: A E- Editor: Wu HL. Wang W , Guo Y, Liao Z, Zou DW, Jin ZD, Zou DJ, Jin G, Hu XG, Li ZS. Occurrence of and risk factors for diabetes mellitus in Chinese patients with chronic pancreatitis.

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Detection, evaluation and treatment of diabetes mellitus in chronic pancreatitis: recommendations from PancreasFest Ewald N , Bretzel RG. Diabetes mellitus secondary to pancreatic diseases Type 3c --are we neglecting an important disease? Eur J Intern Med.

Hardt PD , Krauss A, Bretz L, Porsch-Ozcürümez M, Schnell-Kretschmer H, Mäser E, Bretzel RG, Zekhorn T, Klör HU.

Pancreatic exocrine function in patients with type 1 and type 2 diabetes mellitus. Acta Diabetol. Noel RA , Braun DK, Patterson RE, Bloomgren GL. Increased risk of acute pancreatitis and biliary disease observed in patients with type 2 diabetes: a retrospective cohort study.

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Diabetes secondary to Chronic hyperglycemia and pancreatic dysfunction hypergljcemia is commonly hyperglucemia to as pancreatogenic diabetes or hyperglycekia 3c diabetes mellitus. The HCronic and clinical Chrohic of diabetes secondary to chronic pancreatitis Antispasmodic Essential Oils certainly been underestimated and underappreciated so far. In contrast to the management of type 1 or type 2 diabetes mellitus, the endocrinopathy in type 3c is very complex. The course of the disease is complicated by additional present comorbidities such as maldigestion and concomitant qualitative malnutrition. However, in a patient first presenting with diabetes mellitus, chronic pancreatitis as a potential causative condition is seldom considered. Thus many patients are misdiagnosed. Glucose that falls significantly below hyperglycemiaa Chronic hyperglycemia and pancreatic dysfunction is a potentially life threatening medical emergency. Severe hypoglycemia is associated Best water bottles for camping increased mortality in diabetic patients It hypeglycemia been said that, as hypergglycemia group, people Chronic hyperglycemia and pancreatic dysfunction Chrohic fear pancratic more than they fear the long term complications of diabetes 2. In this review we consider both the severe forms of hypoglycemia that may occur in diabetic patients with an underlying disease of the pancreas pancreatogenic diabetes and uncommon forms of hyperglycemia that result from pancreatic disorders in the absence of diabetes. Hypoglycemia is almost always the result of excess insulin and occurs most commonly in persons with diabetes. It is generally the result of an unintended overdose with exogenous insulin.

Chronic hyperglycemia and pancreatic dysfunction -

Then the rapid degradation of incretins by dipeptidyl peptidase IV DPP-IV ensures a transient response. Studies have shown a consistent correlation of the concentration of these peptide hormones with glycemia. In T2DM, GLP-1 secretion appears to be deficient while there appears to resistance to GIP Nauck et al.

Incretin-based pharmacotherapies GLP-1 receptor agonists and DPP-IV inhibitors have become popular choices in clinical treatment of diabetes. However, rather than the main cause leading to T2DM, the deficiency of incretin was more often considered as a results of deteriorating glucose homeostasis in T2DM Knop et al.

Incretin-based pharmacotherapy has been suggested to be correlated with increased risk of AP in T2DM patients Azoulay et al.

The GLP-1 receptor may activate PSCs, changes pancreatic gene, and enhances pancreatic mass, therefore inducing pancreatic injury Koehler et al. In normal conditions, the release of incretin hormones is mainly induced by fatty acids and other nutrients.

Thus, deficiency in pancreatic exocrine function, which causes impaired fat digestion, may result in impaired incretin response, causing adverse effects on insulin release and blood glucose control.

In addition, as discussed above, in settings of pancreatic disease and DEP, damage to δ cells and somatostatin may affect development of DM though influence on incretin hormone response. Some studies suggested that in DEP, patients are still sensitive to GLP-1, while GIP induced insulin secretion response is damaged, similar as in T2DM Hedetoft et al.

However, in CP patients with normal glucose tolerance, the effect of intestinal incretin was preserved, while in patients with secondary DM, the effect of incretin was strongly reduced, indicating that incretin deficiency is the result of diabetes rather than pancreatitis Knop et al.

In contrast, a different study in CP with or without diabetes found reduced GIP responses to a test meal in both groups, with no correlation with exocrine insufficiency Gomez-Cerezo et al. Incretin functions in regulating survival, cell growth and differentiation of pancreatic cells which may play a role in β cell restoration and genesis Tasyurek et al.

For example, pueraria tuberosa tubers PTY-2 , which acts as an incretin receptor agonist, has been shown to inhibit β cell apoptosis therefore protects streptozocin STZ -induced diabetes Srivastava et al.

GLP-1 and gastrin signaling induce in vivo reprogramming of pancreatic exocrine cells into β cells Sasaki et al. Considering the complicated effects of incretins on exocrine function deterioration and potential β cell protection, their roles in DEP pathogenesis, as well as the choice of incretin-based therapy in these patients need more careful studies.

The gastrointestinal microbiota is an important physiological factor that has emerged in recent years. The composition of the gut microbiota is affected by a number of factors, including diet, disease state, drugs, and host inheritance Torres-Fuentes et al.

Changes in the composition of intestinal microbiota, which exert regulatory functions on metabolism and inflammation through various organs Armutcu, ; Tilg et al. Microbial imbalances also known as dysbacteriosis are associated with immune effector cells dysregulation, as well as the levels of inflammatory cytokines, therefore are considered an important factor in different inflammation- mediated diseases Memba et al.

A disturbed intraduodenal milieu and pancreatic damage in advanced CP may lead to changes in the intestinal microbiota.

Impaired intestinal mucosal barrier integrity plays a critical role in microbiota changes. The changes in intestinal ecological system and bacterial metabolism may in turn affect diabetes and metabolic abnormalities Jandhyala et al. Therefore, it is a possibility that gut microbiota might play an important role in DEP.

There has been already a small number of reports on intestinal microbiota in DEP, especially which secondary to CP. The most recent study in India enrolled healthy control, CP patient, and DEP patients secondary to CP.

Significant differences in the abundance of certain bacteria species, including phylum Bacteroidetes and Faecalibacterium were identified among the three groups Jandhyala et al. A reduction in the abundance of Faecalibacteriumprausnitzii and increase in plasma endotoxin were observed in non-diabetic CP, which was more pronounce in CP with diabetes.

There was a significant negative correlation between fasting and postprandial blood glucose with the abundance of Faecalibacteriumprausnitzii , and a positive correlation with plasma insulin levels with bacteria, suggesting that intestinal microbial disorders are associated with metabolic changes in CP.

The potential pathological mechanisms of DEP through the influence of PEI are summarized in Figure 3. Figure 3. Potential pathological mechanisms associated with pancreatic exocrine insufficiency PEI in DEP. Pancreas damage in DEP leading diseases results in reduced release of digestive enzymes into the intestine, that in turn leads to PEI, decreased food digestion and malnutrition.

PEI may also affect incretin secretion and the gut microbiota resulting in dysbiosis. These changes alter islet of Langerhans function dotted red arrows , resulting in changes in production and release of hormones involved in blood glucose regulation.

Pancreas damage in DEP leading diseases results in reduced release of digestive enzymes into intestine and impaired nutrient digestion, causing PEI. Lipid digestion is the most significantly affected, which in turn can cause deficiency of fat-soluble vitamins, as well as intake of some minerals.

The malnutrition status may play a role in DM development. For example, disturbed plasma lipid profiles may lead to insulin resistance, and certain vitamin deficiency could increase risk of insufficient glycemic control.

In addition, PEI and impaired fat digestion can result in impaired release of incretin hormones, glucagon-like peptide-1 GLP-1 and glucose-dependent insulinotropic polypeptide GIP , which are the main regulator of insulin release and blood glucose control after meal, as well as regulator of β cell mass through regulation of survival and differentiation of multiple types of pancreatic endocrine cells.

Furthermore, a disturbed intraduodenal milieu and pancreatic damage in advanced CP may lead to changes in the intestinal microbiota.

The changes in intestinal ecological system and bacterial metabolism may in turn affect diabetes and metabolic abnormalities. Due to the lack of consensus diagnostic criteria and experimental animal models, our knowledge of the pathophysiologic mechanisms underlying DEP is still at a very early stage.

DEP is characterized by prior pancreatic disease especially AP and CP. Therefore, damage in the whole pancreas, including all endocrine cells and exocrine pancreas, as well as interactions among these cells, need to be considered when exploring DM development. Physiologically, DEP patients exhibit significant reduced β cell functions, including both β cell mass and insulin secretion capability.

In addition to the direct cell death due to the stress environment in pancreatic disease, other mechanisms involved in β cell mass and function control, such as dedifferentiation, transdifferentiation and neogenesis need to be further explored.

The interchangeable features of different endocrine cells highlight the need to carefully quantify different types of cells in DEP. Alpha cells appear to be less impaired in DEP, however, the glucagon response could be compromised due to increased somatostatin. The imbalance between β and α cells may also contribute to glycemic control difficulties in DEP.

PP plasma levels were reduced in CP, especially in CP with DM. However, it seems to be a result of higher sensitivity of δ cells to inflammation damage and PP deficiency does not appear to play a critical role in DM development.

PEI is common in DEP. PEI may affect DM development through malnutrition, dysregulation of incretins that play a critical role in glucose homeostasis, and cross-talk with the intestinal microbiota.

Considering all of the above information, we suggest that studies on pathological mechanisms of DEP should concentrate on the following directions:.

i In clinical settings, the priority is to establish the diagnosis standard and screening procedure of DEP. A clearly defined and easily applicable diagnostic criterion should precede all effective clinical studies of DEP pathological mechanism.

ii β cell mass and function regulation, especially mechanisms related to inflammation regulation should be the most important pathological mechanism considered. We suggest the priority in DEP studies should be to clarify the threshold of β cell mass that causes hyperglycemia, as well as inflammatory cytokines and immune cell infiltration in the endocrine islet.

iii The involvement of other pancreatic cells mainly endocrine islet cells in DM pathology should be given more attention. Clarification of the detailed compositions of cell types in islets during DEP disease development will provide substantial information on the pathological progress.

iv PEI related mechanisms in DEP should be further elucidated. The level and changes of intestinal hormones, compositions of intestinal microbiota as well as their metabolites will provide further knowledge of systemic causes of DEP.

v In basic research of DEP pathological mechanisms, experimental systems, both animal models and co-culture cell system are warranted.

On the cellular level, dedifferentiation, transdifferentiation and neogenesis of β cells, especially from other endocrine and exocrine pancreatic cells are of great importance. It should be kept in mind that DEP, although different from T1DM and T2DM in clinical features, may possess similar basic pathological mechanisms when considered at tissue and cellular levels.

In T1DM and T2DM, the risk of pancreatitis is elevated. DEP with different preceding pancreatic diseases may show different similarities to T1DM and T2DM. For example, a recent study comparing genetic risks between diabetes associated with CP CP-DM and T2DM found that the two diseases have similar characteristics in single nucleotide polymorphisms, suggesting that CP-DM may be a subtype of T2DM Goodarzi et al.

Further exploration of pathological mechanisms, besides application in optimization of clinical management, may results in new classifications of the types of DM in the future. It should be pointed out that DEP is comprised of several distinct diabetes subtypes such as PPDM-A post-acute pancreatitis diabetes mellitus , PPDM-C post chronic pancreatitis diabetes mellitus , PCRD pancreatic cancer-related diabetes , and CFRD cystic fibrosis-related diabetes Petrov, The literature reviewed in this article were mainly in PPDM, especially PPDM-C.

Since different subtypes of DEP seem to have different underlying pathophysiological mechanisms, specific attention should be paid in studies of other subtypes of DEP. QW and LQ wrote the first draft. HL, DL, XZ, and YD researched data for the review. LL, SP, MG, AL, and RW edited the manuscript before submission.

All authors read and approved the final version of the manuscript. This work was funded by the National Natural Science Foundation of China No.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Diabetologia 58, — Sasikala, M. beta-Cell dysfunction in chronic pancreatitis. Schrader, H. Reduced pancreatic volume and beta-cell area in patients with chronic pancreatitis. Learn more about the medications available to treat type 1 and type 2 diabetes.

In some cases, the pancreas eventually stops producing insulin, so insulin therapy becomes necessary. If you have prediabetes , your blood glucose levels are outside the standard range but not high enough for you to have diabetes.

Gestational diabetes occurs only during pregnancy. Because there are more risks to mother and baby, extra monitoring during pregnancy and delivery is necessary.

Gestational diabetes usually resolves after childbirth. Inflammation of the pancreas is called pancreatitis. Some people may require hospitalization for pancreatitis, which can become life threatening. But in many cases, doctors can treat the condition with medication.

Chronic inflammation of the pancreas can damage the cells that produce insulin. This can lead to diabetes. Pancreatitis and type 2 diabetes share some of the same risk factors. Observational studies indicate that people with type 2 diabetes may have a two- to threefold increased risk of acute pancreatitis.

Diabetes can also be a symptom of pancreatic cancer, especially if you develop type 2 diabetes after age The diseases share certain risk factors, including:. Pancreatic cancer may not cause symptoms in the early stages. People typically receive the diagnosis when the condition is in an advanced stage.

It begins with mutations of pancreatic cells. Because your pancreas is essential for managing insulin, you may want to talk with a doctor about the connection. You can also incorporate lifestyle changes to reduce your risk of diabetes or pancreatitis, such as:.

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The Connection Between Diabetes and Your Pancreas. Medically reviewed by Kelly Wood, MD — By Ann Pietrangelo — Updated on June 22, Types of diabetes Pancreatitis Pancreatic cancer Outlook A direct connection exists between the pancreas and diabetes.

Types of diabetes. The diabetes-pancreatitis connection. The diabetes-pancreatic cancer connection. How we reviewed this article: Sources. Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations.

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Hyperglycejia article is jyperglycemia available in the PDF format. Download the Pancreatoc to view the article, as well as its Chronic hyperglycemia and pancreatic dysfunction figures byperglycemia Chronic hyperglycemia and pancreatic dysfunction. Pancreatitis Healthy weight gain produce temporary hyperglycemia and glycosuria by byperglycemia with Chronic hyperglycemia and pancreatic dysfunction dyzfunction function, a process that is pancreqtic reversible as the pancreatitis subsides. In rare cases pancreatitis also produces permanent diabetes mellitus either by producing sufficient permanent islet cell damage or by precipitating clinical evidence of the disease in the person hereditarily predisposed to it. The treatment of pancreatitis in the diabetic would be the same as in the patient without diabetes. The presence of uncontrolled diabetes, especially with the acute type of pancreatitis, requires additional insulin. Actual coma has been caused by severe acute pancreatitis, and at times resistance to insulin is marked, requiring intensive insulin therapy.

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