Insulin Basics
Diabetics need insulin therapy because they can't make their own. Insulin therapy tries to mimic natural insulin secretion — what happens automatically in non-diabetics. The ultimate goal of insulin therapy is to mimic normal insulin levels. Unfortunately, current insulin replacement therapy can only approximate normal insulin levels. Insulin therapy for type 2 diabetes ranges from one injection a day to multiple injections and using an insulin pump (continuous subcutaneous insulin infusion – CSII). The more frequent the insulin injections, the better the approximation of natural or normal insulin levels. Discuss with your medical provider the insulin regimen that is best for you. On this page you will learn about: Normal or Non-diabetic blood sugar levels and insulin release from the pancreas Natural insulin (i.e. insulin released from your pancreas) keeps your blood sugar in a very narrow range. Overnight and between meals, the normal, non-diabetic blood sugar ranges between 60-100mg/dl and 140 mg/dl or less after meals and snacks. See the picture below of blood sugar levels throughout the day in someone who does not have diabetes. To keep the blood sugar controlled overnight, fasting and between meals, your body releases a low, background level of insulin. When you eat, there is a large burst of insulin. This surge of insulin is needed to dispose of all the carbohydrate or sugar that is getting absorbed from your meal. All of this happens automatically! More About Natural Insulin Release Insulin is continuously released from the pancreas into the blood stream. Although the insulin is quickly destroyed (5-6 minutes) the effect on cells may last 1-1/2 hours. When your body needs more insulin, the blood levels quickly rise, and, the converse – when you need less, Continue reading >>
Estimation Of Plasma Insulin And Endogenous Insulin Secretion In Critically Ill Patients Using Intensive Control Insulin-nutrition-glucose Model
The objective of this study is to estimate total plasma insulin level and endogenous insulin secretion by using Intensive Control Insulin-Nutrition-Glucose (ICING) model and 90 critically ill patients data from Hospital Tengku Ampuan Afzan, Kuantan. Integral-based method wasapplied to solve mathematical equations defined in ICING model to find critical parameters of insulin sensitivity (SI) and results of total endogenous insulin secretion and total plasma insulin level were presented in median and 95% confidence interval (CI). It is reported that thetotal median plasma insulin is 1.35 106 mU while (6.59 105, 2.79 106) mU is in 95% CI, and the total median endogenous insulin secretion is 12.9% from the total median plasma insulin. The results elucidated the effectiveness of currentpractice via Intensive Insulin Infusion Therapy (IIT) and also suggest a further study on investigating the incretin mechanism which is strongly believed to contribute to the total plasma insulin level and help to simulate endogenous insulin secretion. No Reference information available - sign in for access. No Citation information available - sign in for access. Keywords: Critically Ill ; Endogenous Insulin ; Exogenous Insulin ; ICING Model ; Plasma Insulin Affiliations:1: Human Engineering Focus Group (HEG), Universiti Malaysia Pahang, 26600 Pekan, Pahang, Malaysia 2: Advanced Medical and Dental Institute, Universiti Sains Malaysia, Bertam, 13200 Kepala Batas, Pulau Pinang, Malaysia 3: College of Engineering, UNITEN, KM7, Jalan Ikram UNITEN, 43000 Kajang, Selangor, Malaysia 4: Department of Anaesthesiology and Intensive Care, Kuliyyah of Medicine, International Islamic University Malaysia, Bandar Indera Mahkota Campus, Jalan Sultan Ahmad Sha, 25200 Kuantan, Pahang, Malaysia ADVANCED SCIENCE Continue reading >>
- NIHR Signal Insulin pumps not much better than multiple injections for intensive control of type 1 diabetes
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
- Type 2 Diabetes Remission With Intensive Treatment
C-peptide In Type 1 Diabetes
Synthesis and secretion Preproinsulin, the transcriptional product of the insulin gene, is produced in the endoplasmic reticulum of the beta cell. Microsomal enzymes cleave preproinsulin to proinsulin, which contains the insulin alpha and beta chains, linked by a connecting peptide, C-peptide. Proinsulin is then transported to the Golgi complex, where it is packaged within clathrin-coated secretory granules. C-peptide is essential for the correct folding of proinsulin by forming two disulphide bridges between cysteine residues of the alpha and beta chains and one within the alpha chain. Following maturation, the secretory granule loses its clathrin coat and proinsulin undergoes proteolytic cleavage and further processing into insulin and C-peptide, which are co-secreted in equimolar amounts into the portal circulation. Once C-peptide is cleaved, the terminal end of the beta chain can bind to the insulin receptor.[1] C-peptide metabolism C-peptide is removed from the peripheral circulation at a constant rate. It is metabolised in the proximal renal tubules, and about 5–10% is excreted unchanged in the urine . Biological role Although traditionally considered to be biologically inert, there is some evidence that C-peptide has active properties. It binds to a membrane structure, probably a G-protein coupled membrane receptor, eliciting a rise in intracellular Ca2+ concentration and subsequent activation of at least two enzyme systems, Na+,K+ ATPase and endothelial nitric oxide synthase (eNOS). C-peptide administration leads to increased blood flow in skeletal muscle and skin, diminished glomerular hyperfiltration, reduced urinary albumin excretion and improved nerve function in patients with type 1 diabetes who lack C-peptide, but not in healthy subjects. It has therefor Continue reading >>
Assessment Of Endogenous Insulin Secretion In Insulin Treated Diabetes Predicts Postprandial Glucose And Treatment Response To Prandial Insulin
Assessment of endogenous insulin secretion in insulin treated diabetes predicts postprandial glucose and treatment response to prandial insulin Jones et al.; licensee BioMed Central Ltd.2012 In patients with both Type 1 and Type 2 diabetes endogenous insulin secretion falls with time which changes treatment requirements, however direct measurement of endogenous insulin secretion is rarely performed. We aimed to assess the impact of endogenous insulin secretion on postprandial glucose increase and the effectiveness of prandial exogenous insulin. We assessed endogenous insulin secretion in 102 participants with insulin treated diabetes (58 Type 1) following a standardised mixed meal without exogenous insulin. We tested the relationship between endogenous insulin secretion and post meal hyperglycaemia. In 80 participants treated with fast acting breakfast insulin we repeated the mixed meal with participants usual insulin given and assessed the impact of endogenous insulin secretion on response to exogenous prandial insulin. Post meal glucose increment (90 minute - fasting) was inversely correlated with endogenous insulin secretion (90 minute C-peptide) (Spearmans r = 0.70, p < 0.001). Similar doses of exogenous prandial insulin lowered glucose increment more when patients had less endogenous insulin; by 6.4(4.2-11.1) verses 1.2(0.03-2.88) mmol/L (p < 0.001) for patients in the lowest verses highest tertiles of endogenous insulin. In insulin treated patients the measurement of endogenous insulin secretion may help predict the degree of postprandial hyperglycaemia and the likely response to prandial insulin. DiabetesC-peptidePostprandialGlucoseInsulin Guidelines for treatment in Type 1 and Type 2 diabetes differ greatly predominantly reflecting differences in endogenous ins Continue reading >>
- Postprandial Blood Glucose Is a Stronger Predictor of Cardiovascular Events Than Fasting Blood Glucose in Type 2 Diabetes Mellitus, Particularly in Women: Lessons from the San Luigi Gonzaga Diabetes Study
- Why Isn't Postprandial Insulin Assay Being Used to Predict Diabetes Onset?
- Glucose response holds key to better obesity and diabetes drugs
What Is The Diference Between Endogenous Insulin And Exogenous Insulin?
Endogenous insulin is the insulin your pancreas makes which means it is coming from your body. Exogenous would be like giving someone insulin-a type I diabetic who no longer makes insulin would need exogenous insulin to keep blood sugars under control. Now, Type I and Type II are treated very differently and should be. Treatment of Type II should always be holding off on medications or insulin for as long as possible because research has shown that by taking over the job of endogenous insulin, you are actually speeding up the process of the need for exogenous insulin because your bodies metabolic pathways are activated at a different rate and learn to be utilized faster by bypassing the normal route as if someone did not have diabetes. It is always exercise and diet control first, then possibly mediations but with continued diet and exercise. Also, keeping medications at the lowest doses possible. Keeping in mind, stress, hormones, thyroid, illness, etc can all raise blood glucose and the Hemoglobin A1c is not able to be used to decipher is someone is a diabetic. The A1c looks at your sugar levels over 3-4 months. The best way to keep control of your sugars is carb counting, not fun and time consuming but worth it in the long run. Continue reading >>
What Is Exogenous Insulin?
By Elisabeth Almekinder RN, BA, CDE Leave a Comment To understand what exogenous insulin means, one must go back to the Greek root of the word. Exo means out of, or external,. Exogenous insulin literally means insulin that comes from outside. Speaking of exogenous insulin can provoke fear and anxiety for people with Type 2 diabetes , who have gone years without having to take insulin from external sources than their body. Often these fears stem from a past experience, with a relative who had diabetes who started insulin therapy, and as a result, later had lower limb amputation, or other diabetes complications. Exogenous insulin is then associated with the decline of quality of life, and every effort to avoid it may be undertaken by the person with diabetes. It can also certainly provoke fear and anxiety in a person who is newly diagnosed with Type 1 diabetes. They are faced at once with the reality that all their insulin will now have to come from exogenous sources, because their pancreas no longer manufacture it. Injections, insulin pump set application, and blood sugar checks are all invasive procedures, and the idea that this will be a lifelong endeavor is overwhelming. Patti didnt want to start on insulin. Her Type 2 diabetes had progressed to the point where three different diabetes medications were insufficient in controlling her blood sugars. She was getting frustrated. When she went to see her doctor, Patti was told that she needed to start taking insulin injections. She started combing the internet for information about insulin for Type 2 diabetes. She ran across some research that exogenous insulin for Type 2 diabetes increased complications. When Patti called, she was beside herself with worry. She couldnt control her blood sugar without insulin, but was fea Continue reading >>
Why Is The C-peptide Used Generally Instead Of Insulin In Detection And Qualification Of Functional Beta Cell Situation?
Insulin detection reflects the insulin from outside (exogenous) source, such as insulin injections and inside (endogenous) source that is pancreas, whereas C-peptide test reflects only endogenous insulin. Therefore, C-peptide is mostly used to detect functional beta cell mass. True, you must measure c-peptide if your subject or patient is taking insulin , such as in the case of a pancreas transplant patient who is on insulin post-op or because the graft is not working well. Another reason is that insulin levels drop significantly during the first pass through the liver. This is not the case with C-peptide, so you can get a better measure of actual secretion from C-Peptide. While I was writing my questions I had forgotten something. I had wanted to cell culture situation. For instance, you have differentiated some cell type into beta cell. Namely, you think that. So you add glucose into medium of this new cell which you think differantiaton. And you would detect functionality of this new cell ( if there is beta cell ). But why investigations use the C-peptide?There is insulin in Serum as far as I know even if low level. n that case, there is no C-peptide in serum ? But how can it be ? C-peptide is released into blood ? If a cell line secretes insulin, it will also secrete c-peptide. You can check the level of insulin and/or c-peptide in your serum, but it is not really necessary for secretion studies unless you are performing the studies using serum supplemented media, as opposed to some buffer system such as Krebs-Ringer with BSA. Circumstance that in secretion or in cell, So what ? Birefly and briefly, I wonder and I ask that short question. C-peptide is generally used to detect beta cell in ''''' cell culture, so, in cell, in single beta cell ''''. In immunoflorescen Continue reading >>
Insulin: Reference Range, Interpretation, Collection And Panels
Insulin is an anabolic hormone that promotes glucose uptake, glycogenesis, lipogenesis, and protein synthesis of skeletal muscle and fat tissue through the tyrosine kinase receptor pathway. In addition, insulin is the most important factor in the regulation of plasma glucose homeostasis, as it counteracts glucagon and other catabolic hormonesepinephrine, glucocorticoid, and growth hormone. Table 1. Reference Range of Insulin Levels [ 1 ] (Open Table in a new window) A standard insulin test is positive for endogenous insulin and exogenous insulin. In addition, there is a minimal cross-reaction with proinsulin and insulinlike growth factors 1 and 2, with the degree of variability depending on the brand of the testing toolkit and technique used. Insulin testing is used to assist in identifying causes of hypoglycemia (plasma glucose levels < 55 mg/dL), especially upon signs and symptoms of hypoglycemia (neurohypoglycopenic and autonomic symptoms). In this scenario, a 72-hour fasting test is performed. [ 2 ] Insulinoma: High insulin and C-peptide levels Nonbeta cell tumors: Low insulin and C-peptide levels and high insulinlike growth factor 2 level [ 3 ] Excessive insulin administration: High insulin levels and low C-peptide levels Insulin secretagogue administration (sulfonylurea and glinides): High insulin and C-peptide levels Congenital hyperinsulinism (mutation in insulin-secreting gene): High insulin and C-peptide levels Autoimmunity to insulin or insulin receptor (common in patients receiving insulin or those who have autoimmune diseases such as systemic lupus erythematosus [SLE] or Hashimoto thyroiditis): Postprandial insulin is bound to antibodies and dissociated 1 hour later, resulting in an extremely elevated insulin level and high insulintoC-peptide ratio [ 4 ] T Continue reading >>
- The interpretation and effect of a low-carbohydrate diet in the management of type 2 diabetes: a systematic review and meta-analysis of randomised controlled trials
- Assessing how controlled is your diabetes: hba1c range
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
Drugs To Increase Insulin Production
Diabetes is a group of diseases that cause high blood sugar (glucose) levels. The high blood glucose levels are caused by problems in insulin production or function. Insulin is a hormone released by the pancreas when you eat food. It allows sugar to move from the blood into the cells, where it’s used for energy. If the cells of the body aren’t using insulin well, or if the body is unable to make enough insulin, glucose can build up in the blood. The increase in blood glucose levels may lead to uncomfortable symptoms, such as: constant thirst increased urination excessive hunger unintentional or unexplained weight loss fatigue or lack of energy irritability blurry vision wounds that heal more slowly than normal recurring or frequent infections There are two main types of diabetes. Type 1 diabetes develops when the body doesn’t make any insulin. It’s most often diagnosed during childhood, but it may be diagnosed later in life. Type 2 diabetes occurs when the body doesn’t produce enough insulin or doesn’t use insulin properly. It’s more commonly seen in adults, but the number of children with type 2 diabetes is increasing. Both types of diabetes cause a buildup of glucose in the bloodstream. This can lead to serious health problems, including: vision loss kidney damage skin problems hearing impairment heart disease stroke blood circulation problems limb amputation Most of these complications are preventable with treatment. Treatment plans for diabetes often involve monitoring blood glucose levels, following a healthy diet, and taking medications. Many of these medications work by raising the body’s insulin levels. Increased insulin production helps deliver the glucose in your blood to your cells. This prevents glucose from building up in your bloodstream. N Continue reading >>
Insulin
This article is about the insulin protein. For uses of insulin in treating diabetes, see insulin (medication). Not to be confused with Inulin. Insulin (from Latin insula, island) is a peptide hormone produced by beta cells of the pancreatic islets, and it is considered to be the main anabolic hormone of the body.[5] It regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of, especially, glucose from the blood into fat, liver and skeletal muscle cells.[6] In these tissues the absorbed glucose is converted into either glycogen via glycogenesis or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both.[6] Glucose production and secretion by the liver is strongly inhibited by high concentrations of insulin in the blood.[7] Circulating insulin also affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve body fat. Beta cells are sensitive to glucose concentrations, also known as blood sugar levels. When the glucose level is high, the beta cells secrete insulin into the blood; when glucose levels are low, secretion of insulin is inhibited.[8] Their neighboring alpha cells, by taking their cues from the beta cells,[8] secrete glucagon into the blood in the opposite manner: increased secretion when blood glucose is low, and decreased secretion when glucose concentrations are high.[6][8] Glucagon, through stimulating the liver to release glucose by glycogenolysis and gluconeogenesis, has the opposite effect of insulin.[6][8] The secretion of insulin and glucagon into the Continue reading >>
Insulin Resistance: Definition And Clinical Spectrum
INTRODUCTION Insulin resistance can be broadly defined as a subnormal biological response to normal insulin concentrations. By this definition, it may pertain to many biological actions of insulin in many tissues of the body. Typically, however, in clinical practice, insulin resistance refers to a state in which a given concentration of insulin is associated with a subnormal glucose response [1]. The term first came into use several years after the introduction of insulin therapy in 1922 to describe occasional diabetic patients who required increasingly large doses of insulin to control hyperglycemia. Most of these patients developed insulin resistance secondary to antibodies directed against the therapeutic insulin, which at that time was both impure and derived from non-human species [2]. Antiinsulin antibodies are rare in patients treated with recombinant human insulin, and the spectrum of clinical disorders in which insulin resistance plays a major role has changed markedly. Insulin resistance, rather than being a rare complication of the treatment of diabetes, is now recognized as a component of several disorders, including the following (table 1): Extreme insulin-resistance syndromes, such as the type B syndrome with autoantibodies against the insulin receptor [3], and rare inherited disorders, such as Leprechaunism with insulin-receptor mutations [4] and the lipodystrophic states [5]. Impaired glucose tolerance and type 2 diabetes mellitus. Obesity, stress, infection, uremia, acromegaly, glucocorticoid excess, and pregnancy, which cause secondary insulin resistance. Common disorders such as the metabolic syndrome, hypertension, hyperlipidemia, coronary artery disease, the polycystic ovary syndrome (PCOS), and ovarian hyperthecosis, in which the mechanism of the a Continue reading >>
Endogenous Insulin Secretion Even At A Very Low Level Contributes To The Stability Of Blood Glucose Control In Fulminant Type 1 Diabetes
Endogenous insulin secretion even at a very low level contributes to the stability of blood glucose control in fulminant type 1 diabetes We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Endogenous insulin secretion even at a very low level contributes to the stability of blood glucose control in fulminant type 1 diabetes Saeko Shibasaki, Akihisa Imagawa, [...], and Toshiaki Hanafusa Fulminant type 1 diabetes is characterized by almost complete cell destruction, resulting in scarce insulin secretion. In the present study, we aimed to clarify clinical features related to serum Cpeptide levels measured by a high sensitivity method, chemiluminescent enzyme immunoassay, in 12 patients with fulminant type 1 diabetes. Serum Cpeptide was detected (0.0070.10 nmol/L) in four patients and was not detected in eight patients. A negative correlation was observed between serum Cpeptide levels and daily dosages of insulin (P < 0.01). The patients with detectable Cpeptide showed a significantly lower Mvalue than those without (P = 0.01). In conclusion, our present results suggest that even very low levels of endogenous insulin secreting capacity can improve daily dosages of insulin and stabilize blood glucose levels. (J Diabetes Invest, doi: 10.1111/j.20401124.2010.0059.x, 2010) Keywords: Fulminant type 1 diabetes, Serum Cpeptide, Mvalue Type 1 diabetes is characterized by insulin deficiency resulting from destruction of pancreatic cells and subc Continue reading >>
Interaction Between Exogenous Insulin, Endogenous Insulin, And Glucose In Type 2 Diabetes Patients.
Diabetes Technol Ther. 2015 May;17(5):335-42. doi: 10.1089/dia.2014.0326. Epub 2015 Mar 18. Interaction between exogenous insulin, endogenous insulin, and glucose in type 2 diabetes patients. 1 Department of Endocrinology and Internal Diseases, Aarhus University Hospital , Aarhus, Denmark . Little is known about the influence of exogenous insulin and actual glucose levels on the release of endogenous insulin in insulin-treated type 2 diabetes mellitus (T2DM) patients. This study investigated the interaction among serum endogenous insulin (s-EI), serum exogenous insulin aspart (s-IAsp), and blood glucose levels in an experimental short-term crossover design. Eight T2DM patients (63.52 years old; range, 49-69 years; mean body mass index, 28.83.8 kg/m(2)) were randomized to treatment with individual fixed doses of insulin aspart (0.5-1.5 IU/h) as a continuous subcutaneous insulin infusion (CSII) during a 10-h period on two occasions with different duration of hyperglycemia: (1) transient hyperglycemia for 2 h (visit TH) and (2) continuous hyperglycemia for 12 h (visit CH). During steady state the variances of plasma glucose (p-glucose), s-IAsp, and s-EI were equal within visit TH and within visit CH, but variances were significantly higher during visit CH compared with visit TH. The s-IAsp reached lower levels at visit CH compared with visit TH (test for slope=1, P=0.005). The s-EI depended on p-glucose in a nonlinear fashion during the first 100 min of both visits when s-IAsp was undetectable (adjusted R(2)=0.9). A complex but statistically significant interaction among s-IAsp, s-EI, p-glucose, and patients was observed during measurable s-IAsp levels (adjusted R(2)=0.70). Endogenous and exogenous insulin showed higher variation during continuous hyperglycemia. Significa Continue reading >>
Relationship Between Insulin Resistance And An Endogenous Nitric Oxide Synthase Inhibitor
Context Increased levels of asymmetric dimethylarginine (ADMA) are associated with endothelial dysfunction and increased risk of cardiovascular disease. Several cardiovascular risk factors are associated with reduced sensitivity to insulin, but elevated ADMA concentrations have not been fully linked to the metabolic syndrome. Objective To evaluate the relationship between insulin sensitivity and plasma ADMA concentrations, and to determine whether a pharmacological treatment that increases insulin sensitivity would also modulate ADMA concentrations. Design, Setting, and Subjects Cross-sectional study, containing a nonrandomized controlled trial component, of 64 healthy volunteers without diabetes (42 women, 22 men; 48 with normal blood pressure and 16 with hypertension), which was conducted at a university medical center between October 2000 and July 2001. Intervention Rosiglitazone (4 mg/d for 4 weeks and then 4 mg twice daily for 8 weeks), an insulin-sensitizing agent, was given to 7 insulin-resistant subjects with hypertension. These subjects were studied before and after 12-week treatment. Main Outcome Measures Insulin sensitivity measured by the insulin suppression test, and fasting plasma levels of low-density lipoprotein cholesterol, triglycerides, high-density lipoprotein cholesterol, glucose, insulin, and ADMA concentrations. Results Plasma ADMA concentrations were positively correlated with impairment of insulin-mediated glucose disposal in nondiabetic, normotensive subjects (r = 0.73; P<.001). Consistent with the metabolic syndrome, ADMA levels were also positively correlated with fasting triglyceride levels (r = 0.52; P<.001) but not with low-density lipoprotein cholesterol levels (r = 0.19; P = .20). Plasma ADMA concentrations increased in insulin-resistant Continue reading >>
National Diabetes Education Initiative (ndei) :: Ndei.org Glossary Endogenous Insulin
Shyangdan DS, Royle P, Clar C, Sharma P, Waugh N, Snaith A. Glucagon-like peptide analogues for type 2 diabetes mellitus. Cochrane Database Syst Rev. 2011 Oct 5;(10):CD006423. Glucagon-like peptide analogues are a new class of drugs used in the treatment of type 2 diabetes that mimic the endogenous hormone glucagon-like peptide 1 (GLP-1). GLP-1 is an incretin, a gastrointestinal hormone that is released into the circulation in response to ingested nutrients. Tahrani AA, Bailey CJ, Del Prato S, Barnett AH. Management of type 2 diabetes: new and future developments in treatment. Lancet. 2011;378(9786):182-97. The increasing prevalence, variable pathogenesis, progressive natural history, and complications of type 2 diabetes emphasise the urgent need for new treatment strategies. Lucidi P, Porcellati F, Rossetti P, Candeloro P, Cioli P, Marzotti S, Andreoli AM, Fede R, Bolli GB, Fanelli CG. Pharmacokinetics and Pharmacodynamics of Therapeutic Doses of Basal Insulins NPH, Glargine, and Detemir After 1 Week of Daily Administration at Bedtime in Type 2 Diabetic Subjects: A randomized cross-over study. Diabetes Care. 2011;34(6):1312-4. To compare the pharmacokinetics and pharmacodynamics of NPH, glargine, and detemir insulins in type 2 diabetic subjects. Kim W, Egan JM.The role of incretins in glucose homeostasis and diabetes treatment.Pharmacol Rev.Pharmacol Rev. 2008;60(4):470-512. Incretins are gut hormones that are secreted from enteroendocrine cells into the blood within minutes after eating. One of their many physiological roles is to regulate the amount of insulin that is secreted after eating. In this manner, as well as others to be described in this review, their final common raison d'tre is to aid in disposal of the products of digestion. Boschmann M, Engeli S, Dobbe Continue reading >>
