Type 2 Diabetes And Gastroparesis
Gastroparesis, also called delayed gastric emptying, is a disorder of the digestive tract that causes food to remain in the stomach for a period of time that is longer than average. This occurs because the nerves that move food through the digestive tract are damaged, so muscles don’t work properly. As a result, food sits in the stomach undigested. The most common cause of gastroparesis is diabetes. It can develop and progress over time, especially in those with uncontrolled blood sugar levels. The following are symptoms of gastroparesis: heartburn nausea vomiting of undigested food early fullness after a small meal weight loss bloating loss of appetite blood glucose levels that are hard to stabilize stomach spasms acid reflux Gastroparesis symptoms may be minor or severe, depending on the damage to the vagus nerve, a long cranial nerve that extends from the brain stem to the abdominal organs, including those of the digestive tract. Symptoms can flare up any time, but are more common after the consumption of high-fiber or high-fat foods, all of which are slow to digest. Women with diabetes have a high risk for developing gastroparesis. Other conditions can compound your risk of developing the disorder, including previous abdominal surgeries or a history of eating disorders. Diseases and conditions other than diabetes can cause gastroparesis, such as: viral infections acid reflux disease smooth muscle disorders Other illnesses can cause gastroparesis symptoms, including: Parkinson’s disease chronic pancreatitis cystic fibrosis kidney disease Turner’s syndrome Sometimes no known cause can be found, even after extensive testing. People who have gastroparesis have damage to their vagus nerve. This impairs nerve function and digestion because the impulses needed to chu Continue reading >>
Will You Have Delayed Gastric Emptying With Metformin - From Fda Reports - Ehealthme
A study for a 30 year old man who takes Risperidone NOTE: The study is based on active ingredients and brand name. Other drugs that have the same active ingredients (e.g. generic drugs) are NOT considered. WARNING: Please DO NOT STOP MEDICATIONS without first consulting a physician since doing so could be hazardous to your health. DISCLAIMER: All material available on eHealthMe.com is for informational purposes only, and is not a substitute for medical advice, diagnosis, or treatment provided by a qualified healthcare provider. All information is observation-only, and has not been supported by scientific studies or clinical trials unless otherwise stated. Different individuals may respond to medication in different ways. Every effort has been made to ensure that all information is accurate, up-to-date, and complete, but no guarantee is made to that effect. The use of the eHealthMe site and its content is at your own risk. You may report adverse side effects to the FDA at or 1-800-FDA-1088 (1-800-332-1088). If you use this eHealthMe study on publication, please acknowledge it with a citation: study title, URL, accessed date. Continue reading >>
Effect Of Altered Gastric Emptying And Gastrointestinal Motility On Metformin Absorption
Effect of altered gastric emptying and gastrointestinal motility on metformin absorption 1Department of Metabolism and Pharmacokinetics, Bristol-Myers Squibb Company, Princeton, NJ 08543 2Department of Biostatistics and Data Management, Bristol-Myers Squibb Company, Princeton, NJ 08543, USA and 3Pharmaceutical Profiles Limited, Nottingham, UK Correspondence: Punit H. Marathe, Department of Metabolism and Pharmacokinetics, Bristol-Myers Squibb Company, Princeton, NJ 085434000, USA. Tel.: (609) 252 5256; Fax: (609) 252 3028; E-mail: [email protected] Received 1999 Dec 23; Accepted 2000 Jul 12. This article has been cited by other articles in PMC. The purpose of this in vivo human study was to assess the effect of altered gastric emptying and gastrointestinal motility on the absorption of metformin in healthy subjects. An open-label, three treatment, three period crossover study was conducted in 11 healthy volunteers. Each subject received 550 mg metformin hydrochloride in solution alone; 5 min after a 10 mg i.v. dose of metoclopramide; and 30 min after a 30 mg oral dose of propantheline. Metformin solution was radiolabeled by the addition of 99mTc-DTPA. The gastrointestinal transit of the solution was monitored by gamma scintigraphy and the pharmacokinetic data were correlated with the scintigraphic findings. Scintigraphic data indicated that pretreatment with metoclopramide decreased gastric emptying time and increased gastrointestinal motility while pretreatment with propantheline had the opposite effect. The systemic disposition of metformin was not altered by pretreatment with metoclopramide and propantheline, as judged by unchanged renal clearance and elimination half-life of metformin. Extent of metformin absorption was essentially unchanged after pretreatment with Continue reading >>
Decreased Gastric Motility In Type Ii Diabetic Patients
Decreased Gastric Motility in Type II Diabetic Patients Yi-Chun Chiu ,1 Ming-Chun Kuo ,2 Christopher K. Rayner ,3 Jung-Fu Chen ,2 Keng-Liang Wu ,1 Yeh-Pin Chou ,1 Wei-Chen Tai ,1and Ming-Luen Hu 1 1Division of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan 2Division of Endocrinology & Metabolism, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University, College of Medicine, Kaohsiung, Taiwan 3University of Adelaide, Discipline of Medicine, Royal Adelaide Hospital, Adelaide, SA 5005, Australia Received 14 May 2014; Accepted 18 June 2014; Published 23 July 2014 Copyright 2014 Yi-Chun Chiu et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. To differentiate gastric motility and sensation between type II diabetic patients and controls and explore different expressions of gastric motility peptides. Methods. Eleven type II diabetic patients and health volunteers of similar age and body mass index were invited. All underwent transabdominal ultrasound for gastric motility and visual analogue scales. Blood samples were taken for glucose and plasma peptides (ghrelin, motilin, and glucacon-like peptides-1) by ELISA method. Results. Gastric emptying was significantly slower in diabetic patients than controls (T50: 46.3 (28.052.3) min versus 20.8 (9.622.8) min, ) and less antral contractions in type II diabetic patients were observed . Fundus dimensions did not differ. There were a trend for less changes in gastrointestinal sensations in type II diabetic Continue reading >>
Metformin And Digestive Disorders
Digestive disorders (diarrhoea, vomiting) represent the most common metformin side-effects (around 30%) with this first-line drug treatment for type 2 diabetes. In healthy individuals, metformin affects glucose, vitamin B12 and the digestive uptake of bile salts. In the colon, it acts locally by modifying glucose cell metabolism. Different pathophysiological hypotheses have been proposed to explain the metformin-induced diarrhoea and vomiting, which can sometimes cause the patient to stop an effective treatment. These theories include stimulation of intestinal secretion of serotonin, changes in incretin and glucose metabolism, and bile-salt malabsorption. However, none of these hypotheses can be considered an adequate pathophysiological explanation of metformin digestive side-effects. In addition, there is a lack of experimental data to explain these highly patient-dependent adverse effects. The full text of this article is available in PDF format. Les troubles digestifs (diarrhée, vomissements) sous metformine représentent l’effet indésirable le plus fréquent (environ 30 %) pour le médicament de référence du diabète de type 2. Chez l’individu non diabétique, la metformine agit sur l’absorption digestive du glucose, de la vitamine B12 et des sels biliaires. Pour le côlon, elle agit localement en modifiant le métabolisme cellulaire. Différentes hypothèses physiopathologiques peuvent expliquer les diarrhées et vomissements qui peuvent obliger le patient à cesser un traitement efficace: stimulation de la sécrétion intestinale de sérotonine, modification des incrétines et du métabolisme du glucose ou malabsorption des sels biliaires. Aucune de ces hypothèses ne peut être considérée comme l’explication physiopathologique des effets secondaires Continue reading >>
A popular oral drug for treating Type 2 diabetes. Metformin (brand name Glucophage, Glucophage XR, Glumetza, Riomet) is a member of a class of drugs called biguanides that helps lower blood glucose levels by improving the way the body handles insulin — namely, by preventing the liver from making excess glucose and by making muscle and fat cells more sensitive to available insulin. Metformin not only lowers blood glucose levels, which in the long term reduces the risk of diabetic complications, but it also lowers blood cholesterol and triglyceride levels and does not cause weight gain the way insulin and some other oral blood-glucose-lowering drugs do. Overweight, high cholesterol, and high triglyceride levels all increase the risk of developing heart disease, the leading cause of death in people with Type 2 diabetes. Another advantage of metformin is that it does not cause hypoglycemia (low blood glucose) when it is the only diabetes medicine taken. Metformin is typically taken two to three times a day, with meals. The extended-release formula (Glucophage XR) is taken once a day, with the evening meal. The most common side effects of metformin are nausea and diarrhea, which usually go away over time. A more serious side effect is a rare but potentially fatal condition called lactic acidosis, in which dangerously high levels of lactic acid build up in the bloodstream. Lactic acidosis is most likely to occur in people with kidney disease, liver disease, or congestive heart failure, or in those who drink alcohol regularly. (If you have more than four alcoholic drinks a week, metformin may not be the best medicine for you.) Unfortunately, many doctors ignore these contraindications (conditions that make a particular treatment inadvisable) and prescribe metformin to people Continue reading >>
Can Metformin Cause Delayed Gastric Emptying?
Another effect of Byetta is delayed gastric emptying so ... I don't take Byetta myself, but I try to follow some of the discussions about it because it seems to be related to Amylin/Symlin The same company that makes Byetta also makes Symlin. Symlin (pramlitide) has an amino acid substitution so that it does not form islet amyloid plaque. IAPP is the acronym for islet amylin polypeptide. Amylin is co-secreted with insulin from the pancreatic beta-cells. Some of the effects of Byetta include read more... a reduction in the proinsulin to insulin ratio (so that more of the proinsulin becomes a completed insulin) and first phase insulin tends to be restored. The improved insulin secretion inturn results in suppression of glucagon by insulin and consequently the liver produces less glucose by gluconeogenesis. Another effect of Byetta is delayed gastric emptying so that the carbs If I look at the Byetta prescribing information, there is a substantially greater risk of hypo if someone takes it with metformin or a Sulfonylurea. Don't know if you fall into that category. This may be true of sulfonylureas which simulate insulin secretion, but Continue reading >>
Stopped Metformin-no More Gastroparesis?
Registration is fast, simple and absolutely free so please,join our community todayto contribute and support the site. This topic is now archived and is closed to further replies. I gave it over 3 months: last 6 weeks was increasing nausea constantly, even throughout the night. I finally said "ENOUGH! ...I had allowed enough time for my body's adjustment to Metformin", so I quit it and went back on my Glipizide. Strange thing .....when I quit the Metformin, my Gastroparesis subsided! I haven't had a single episode since I quit the Metformin over 2 weeks ago....and my gastro began around the same time I started Metformin! Hmmmm?/? Yeppers ...totally not 'normal' here! :T Was it really delayed stomach emptying ... or just more generalized nastay indigestion? Will keep that one in mind if I ever develop it ... oh, I am TRULY TRULY fortunate that metformin agrees with me!!! Would be nice if diabetes were a little less 'individual' sometimes. Would be nice if diabetes were a little less 'individual' sometimes. YEAH -- like wouldn't it be nice to eat what the next person does, and be done with it? YEAH -- like wouldn't it be nice to eat what the next person does, and be done with it? Nothing says good times like struggling to manage your own medication over an extended period of time! just out of interest were you taking your metformin AFTER your meals? and how many were you taking? Nothing says good times like struggling to manage your own medication over an extended period of time! And it IS almost invariably managing your own, isn't it! I tried the maximum dose of Metformin for three months to see if it would help with weight loss. I had no side effects, nor any effects for that matter. It did nothing to help the weight loss and made absolutely no difference in my BG numb Continue reading >>
I've been taking Metformin for 2 weeks. I'm up to 1500mg/day in 3 doses. It's causing delayed gastric emptying for me. Food just sits in my stomach for hours. It's not acid reflux or anything, it just feels like I swallowed a brick. Last night it got really bad; 7 hours after a small, low carb dinner, I couldn't sleep because of it, and finally threw up. There was still a lot of food in my stomach 7 hours after a meal (after I threw up, I felt fine and slept well). I've never had any stomach problems before, and I don't like the way it feels. Is this a normal reaction to Metformin or am I just having oddball reactions to meds again? I find on Metformin I have to eat very small meals otherwise I get that bloated uncomfortable feeling. I can only eat half a normal size salad or only 2 ounces of meat at a time. This is why I eat 5 or 6 times a day instead of 2 or 3 bigger meals. I've never thrown up but have had that uncomfortable feeling when I eat a normal amount of food. I think one of Metformin's actions is it blocks some of the carbs from being absorbed. So that food just sits there. What exactly did you eat? 115 pounds, Breast Cancer dx'd 6/16, 6 months of chemo and 6 weeks of radiation 2000 metformin ER, 100 mg Januvia,Glimperide, Prolia, Gabapentin, Meloxicam, Probiotic with a Prebiotic, , Lisinopril, B-12, B-6, Tumeric, Magnesium, Calcium, Vit D, and Occuvite mostly vegan diet, low fat and around 125 carbs a day, walk 5-6 miles every other day and 1 hour of yoga and light weights. Some people just can't take Metformin. Me included, and there are a number of reasons I would like to take it. For me it is likely the delayed stomach emptying that revs up my GERD. T2, self diagnosed 2007. On Levemir, Regular, and Humalog. 3 bouts of retinopathy, hence I keep A1C on th Continue reading >>
Metformin Attenuates Hypoglycaemia Secondary To Dumping Syndrome
Metformin attenuates hypoglycaemia secondary to dumping syndrome S Gonzalez1, N Mizban2, R King2 & C Rajeswaran1 1Pinderfield Hospital Mid Yorkshire NHS Trust, Wakefield, UK; 2Dewsbury District Hospital, Mid Yorkshire NHS Trust, Dewsbury, UK. Dumping syndrome is a common complication following gastric bypass surgery. Rapid gastric emptying in dumping syndrome triggers an inappropriate hyperinsulinaemic response which leads to hypoglycaemia. This can be very disabling and challenging to manage in clinical practice. Here we present a lady with dumping syndrome whose post meal hypoglycaemia improved with metformin. A 42-year-old female presented with eight months history of increasing mood swings, short term memory loss and craving for sugary food. She underwent a Roux-en-Y gastric bypass surgery for morbid obesity 7 years previously which was followed by sustained weight loss. Only past medical illness was vitamin B12 deficiency and she was adequately replaced. Alcohol comsuption was minimal. BMI was 29 kg/m2. Physical examination was unremarkable in particular there was no postural drop in blood pressure. Post prandial capillary blood glucose (CBG) were usually between 1.6 and 2.4 mmol/l. Glucose tolerance test revealed a fasting glucose of 4.6 mmol/l and a 2 h sample of 2.2 mmol/l. All investigations for recurrent hypoglycaemia were normal except for an elevated C-Peptide-2166, Insulin-155 during a hypoglycaemic episode. CT abdomen was reported normal. Therefore, late dumping syndrome was diagnosed. Dietary modification, low glycaemic index food, restriction of fluid intake following a meal and avoidance of physical activity immediately after oral intake was recommended. Octreotide was introduced when she was unable to tolerate acarbose. However, her symptoms remained Continue reading >>
Ursodiol On Insulin Sensitivity, Gastric Emptying And Body Weight With Type 2 Diabetes On Metformin
You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Ursodiol on Insulin Sensitivity, Gastric Emptying and Body Weight With Type 2 Diabetes on Metformin The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. ClinicalTrials.gov Identifier: NCT02033876 Information provided by (Responsible Party): Study Description Study Design Arms and Interventions Outcome Measures Eligibility Criteria Contacts and Locations More Information This study will evaluate whether bile acids are able to increase insulin sensitivity and enhance glycemic control in T2DM patients, as well as exploring the mechanisms that enhance glycemic control. These observations will provide the preliminary data for proposing future therapeutic as well as further mechanistic studies of the role of bile acids in the control of glycemia in T2DM. Background: Intra-jejunal administration of bile acids improves insulin sensitivity. Hypothesis: The bile acid, ursodeoxycholic acid (UDCA) in delayed (ileocolonic)-release formulation, stimulates TGR-5 and FXR receptors in the ileum and colon, increasing the secretion of FGF-19, GLP-1, oxyntomodulin (OXM), and PYY3-36, improving insulin sensitivity and inducing weight loss. Aim: To study the effect of an ileocolonic formulation of UDCA on insulin sensitivity, postprandial plasma glycemia and incretin levels, gastric emptying and body weight in overweight or obese type 2 diabetic subjects on monotherapy with metformin. Study design: This is a single center, placebo-controlled, parallel group, single dose randomized controlled trial to study Continue reading >>
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Delayed Gastric Emptying And Gastric Autoimmunity In Type 1 Diabetes
Abstract OBJECTIVE—Delayed gastric emptying and/or gastrointestinal symptoms occur in 30–50% of diabetic patients. Known contributing factors are autonomic neuropathy and acute hyperglycemia, but the role of gastric autoimmunity has never been investigated, although 15–20% of type 1 diabetic patients exhibit parietal cell antibodies (PCAs). We studied gastric motility in diabetes in relation to PCA status, autonomic nerve function, HbA1c, thyroid-stimulating hormone (TSH), Helicobacter pylori (HP), acid production, and gastric histology. RESEARCH DESIGN AND METHODS—Gastric emptying of solids and liquids (measured by 13C-octanoic acid and 13C-glycine breath tests, respectively) was tested in euglycemic conditions in 42 type 1 diabetic patients (male/female: 29/13; 15 PCA+; mean age 40 ± 15 years; mean HbA1c 7.8 ± 0.9%). Gastrointestinal symptoms, autonomic nerve function (Ewing tests), PCA status (indirect immunofluorescence), gastric histology, and acid secretion (pentagastrin) were assessed. RESULTS—Solid gastric emptying was delayed in 40% and liquid emptying in 36% of patients. Gastric motility did not correlate with symptoms. PCA status, gastric morphology, and acid secretion were similar in those with and without gastroparesis. HbA1c level (β = 1.34, P = 0.011) was the only risk factor for delayed solid emptying in a logistic regression model testing HbA1c, autonomic nerve function, PCA, HP status, age, sex, diabetes duration, and TSH. Half-emptying time for liquids correlated with TSH level (r = 0.83, P < 0.0001) and autonomic neuropathy score (r = −0.79, P = 0.001). CONCLUSIONS—We found that ∼50% of type 1 diabetic patients studied had delayed gastric emptying that did not correlate with symptoms. Gastric autoimmunity did not contribute to diab Continue reading >>
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When Diabetes Leads To A Lazy Stomach: The Goods On Gastroparesis
Gastroparesis doesn’t sound good, and it isn’t. Literally “stomach paralysis,” it is a form of diabetic neuropathy, or nerve damage, that is a common complication of diabetes. The damaged nerve in question is the vagus nerve, named for its vagabond-like wandering nature. The vagus nerve meanders all the way from the brainstem to the colon, controlling heart rate, sweating, gastrointestinal contractions, and various other involuntary, automatic functions on its way. In the case of gastroparesis, it’s the vagus nerve’s control of stomach contractions that’s damaged. The stomach is basically a hollow ball made of muscle that serves as a storage container and mixing bowl for food. It’s about the size of a small melon, but it can stretch to hold nearly a gallon if you really press the issue. In healthy people, wave-like contractions of the stomach, prompted by the vagus nerve, crush and churn your food into small particles and mix it up with enzymes and acids produced by the stomach’s inner lining. Then the stomach contractions, coming along in waves at about three per minute, slowly and evenly propel the pulverized food out through the pyloric valve, which opens just enough to release an eighth of an ounce of food at a time. From there it’s down the small intestine, where the real nutrient absorption occurs. It can take four hours to empty your stomach into your small intestine, especially if you’ve eaten fat, which slows the process down. If the vagus nerve has been damaged by years of high blood sugars, the process hits a snag. The walls of the stomach, paralyzed by the lack of vagus nerve stimulation, don’t make their muscular wave-like contractions. As a result, food just sticks around in the stomach, unpulverized and going nowhere. It may sit an Continue reading >>
Metformin Slow Gastric Emptying
Dumping syndrome occurs when food, especially sugar, moves too fast from the stomach to the duodenumthe first part of the small intestinein the upper gastrointestinal otc viagra (GI) tract. This condition is also called rapid gastric emptying. It is mostly associated with conditions following gastric or esophageal surgery, though itAs documented in the literature, pretreatment with metoclopramide produced an accelerated gastric emptying and reduced small intestinal transit of the metformin solution. Pretreatment with propantheline slowed both gastric emptying and small intestinal transit. The systemic kinetics of metformin were not changed byJan 16, 2016 A novel delayed-release preparation of metformin has recently been shown to improve glycaemic control to a similar extent to immediate-release metformin, but with less systemic exposure. We believe that .. Effect of altered gastric emptying and gastrointestinal motility on metformin absorption. Br J ClinInt J Mol Sci. 2017 Jun 16;18(6). pii: E1282. doi: 10.3390/ijms18061282. Acute Effect of Metformin on Postprandial Hypertriglyceridemia through Delayed Gastric Emptying. Sato D(1), Morino K(2), Nakagawa F(3)(4), Murata K(5), Sekine O(6), Beppu F(7), Gotoh N(8), Ugi S(9), Maegawa H(10). Author information: (1)DivisionDigestive disorders (diarrhoea, vomiting) represent the most common metformin side-effects (around 30%) with this first-line drug treatment for type 2 diabetes. Oesophageal dysmotility, delayed gastric emptying and gastrointestinal symptoms in patients with diabetes mellitus Diabet Med 2007 ; 24 : 1235-1239 [cross-ref].AIMS: The purpose of this in vivo human study was to assess the effect of altered gastric emptying and gastrointestinal motility on the absorption of metformin in healthy subjects. METHODS: An Continue reading >>