Physical Activity And Reduced Occurrence Of Non-insulin-dependent Diabetes Mellitus
Physical activity is recommended by physicians to patients with non-insulin-dependent diabetes mellitus (NIDDM), because it increases sensitivity to insulin. Whether physical activity is effective in preventing this disease is not known. We used questionnaires to examine patterns of physical activity and other personal characteristics in relation to the subsequent development of NIDDM in 5990 male alumni of the University of Pennsylvania. The disease developed in a total of 202 men during 98,524 man-years of follow-up from 1962 to 1976. Leisure-time physical activity, expressed in kilocalories expended per week in walking, stair climbing, and sports, was inversely related to the development of NIDDM. The incidence rates declined as energy expenditure increased from less than 500 kcal to 3500 kcal. For each 500-kcal increment in energy expenditure, the age-adjusted risk of NIDDM was reduced by 6 percent (relative risk, 0.94; 95 percent confidence interval, 0.90 to 0.98). This association remained the same when the data were adjusted for obesity, hypertension, and a parental history of diabetes. The association was weaker when we considered weight gain between the time of college attendance and 1962 (relative risk, 0.95; 95 percent confidence interval, 0.90 to 1.00). The protective effect of physical activity was strongest in persons at highest risk for NIDDM, defined as those with a high body-mass index, a history of hypertension, or a parental history of diabetes. These factors, in addition to weight gain since college, were also independent predictors of the disease. Increased physical activity is effective in preventing NIDDM, and the protective benefit is especially pronounced in persons at the highest risk for the disease. (N Engl J Med 1991; 325:147–52.) Continue reading >>
Tear Function And Ocular Surface Changes In Noninsulin-dependent Diabetes Mellitus☆
Abstract Participants Eighty-eight eyes of 50 noninsulin-dependent diabetes mellitus patients seen at the Department of Ophthalmology, Kobe University School of Medicine, from September 1998 through February 1999, and 40 eyes of 20 healthy control individuals were studied. Intervention All subjects underwent routine ophthalmic examinations, corneal sensitivity measurements, Schirmer test, tear film break-up time (BUT) analysis, and conjunctival impression cytologic analysis. Main outcome measures Patients and control subjects were compared for corneal sensitivity, tear function parameters, goblet cell density, and squamous metaplasia grade. The relation of diabetic peripheral neuropathy, metabolic control, duration of disease, and status of retinopathy to the ocular surface disorder was also noted. Results The mean corneal sensitivity was significantly lower in diabetic patients, diabetic patients with peripheral neuropathy, and poorly controlled diabetes compared with control subjects (P < 0.001). The BUT and Schirmer test values were also significantly lower in the diabetic group, in patients with peripheral neuropathy and poor metabolic control. Impression cytologic analysis showed goblet cell loss and conjunctival squamous metaplasia, both of which again related to peripheral neuropathy, poor diabetic control, and decreased corneal sensitivity. The examined parameters did not relate to duration of disease or status of diabetic retinopathy. Conclusions The ocular surface disease in diabetes is characterized by a disorder of tear quantity and quality, squamous metaplasia, and goblet cell loss, all of which seem to evolve in close proximity to the status of metabolic control and peripheral neuropathy. Continue reading >>
- Women in India with Gestational Diabetes Mellitus Strategy (WINGS): Methodology and development of model of care for gestational diabetes mellitus (WINGS 4)
- Can diabetes be cured? A review of therapies and lifestyle changes
- Eating fresh fruit every day and making lifestyle changes lower the risk of diabetes, study says
Diabetes Mellitus Type 2
Diabetes mellitus type 2 (also known as type 2 diabetes) is a long-term metabolic disorder that is characterized by high blood sugar, insulin resistance, and relative lack of insulin.[6] Common symptoms include increased thirst, frequent urination, and unexplained weight loss.[3] Symptoms may also include increased hunger, feeling tired, and sores that do not heal.[3] Often symptoms come on slowly.[6] Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations.[1] The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon.[4][5] Type 2 diabetes primarily occurs as a result of obesity and lack of exercise.[1] Some people are more genetically at risk than others.[6] Type 2 diabetes makes up about 90% of cases of diabetes, with the other 10% due primarily to diabetes mellitus type 1 and gestational diabetes.[1] In diabetes mellitus type 1 there is a lower total level of insulin to control blood glucose, due to an autoimmune induced loss of insulin-producing beta cells in the pancreas.[12][13] Diagnosis of diabetes is by blood tests such as fasting plasma glucose, oral glucose tolerance test, or glycated hemoglobin (A1C).[3] Type 2 diabetes is partly preventable by staying a normal weight, exercising regularly, and eating properly.[1] Treatment involves exercise and dietary changes.[1] If blood sugar levels are not adequately lowered, the medication metformin is typically recommended.[7][14] Many people may eventually also require insulin injections.[9] In those on insulin, routinely checking blood sugar levels is advised; however, this may not be needed in those taking pills.[15] Bariatri Continue reading >>
- Women in India with Gestational Diabetes Mellitus Strategy (WINGS): Methodology and development of model of care for gestational diabetes mellitus (WINGS 4)
- 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
- Metabolic surgery for treating type 2 diabetes mellitus: Now supported by the world's leading diabetes organizations
Genetic Analysis Of Non-insulin Dependent Diabetes Mellitus In The Gk Rat
Non-insulin dependent diabetes mellitus (NIDDM) is a major public health problem, but its aetiology remains poorly understood. We have performed a comprehensive study of the genetic basis of diabetes in the Goto-Kakizaki (GK) rat, the most widely used animal model of non-obese NIDDM. The genetic dissection of NIDDM using this model has allowed us to map three independent loci involved in the disease. In addition, we identify a major factor affecting body weight, but not glucose tolerance, on chromosome 7 and map a further 10 regions that are suggestive for linkage. We conclude that NIDDM is polygenic and fasting hyperglycaemia and postprandial hyperglycaemia clearly have distinct genetic bases. Karisson, O., Edlund, T., Moss, J.B., Rutter, W.J. & Walker, M.D. A mutational analysis of the insulin gene transcription control region: expression in beta cells is dependent on two related sequences within the enhancer. Proc. Natl. Acad. Sci. USA 84, 8819–8823 (1987). Continue reading >>
Non-insulin-dependent Diabetes Mellitus
Alternative Titles: NIDDM, adult-onset diabetes, maturity-onset diabetes, type 2 diabetes, type 2 diabetes mellitus, type II diabetes, type II diabetes mellitus Learn about this topic in these articles: Assorted References antidiabetic agents causation, symptoms, and treatment soft drinks In tolbutamide …treatment of type II (non-insulin-dependent) diabetes. Tolbutamide stimulates the release of insulin from the pancreas, thereby reducing the concentration of glucose in the blood. Continue reading >>
Diabetes Mellitus Type 2
What is Diabetes Mellitus Type 2? Type 2 Diabetes Mellitus is a condition in which the body fails to metabolise glucose (sugar) correctly. This causes levels of sugar in the blood to increase, a state known as hyperglycaemia. When a person does not have diabetes, a gland called the pancreas produces and secretes a hormone called insulin. The hormone is used by the body’s tissues to metabolise glucose. Usually the amount of insulin secreted increases in relation to the amount of carbohydrate (sugar) a person consumes. In people with type 2 diabetes, insulin secretion from the pancreas often decreases. This is referred to as reduced insulin secretion. In addition the body tissues do not respond adequately to the insulin which is produced. Normally the insulin would be used by the body to draw glucose into the cells, where it could be stored as energy which could be used by the body later (e.g. when exercising or any of the other activities which involve energy expenditure). In type 2 diabetes, the glucose is not taken into the cells. This is referred to as insulin resistance. It causes glucose to stay in the blood stream and hyperglycaemia is the result. Type 2 diabetes mellitus was previously called non-insulin dependent diabetes mellitus (NIDDM) and late onset diabetes mellitus. These names are no longer used because they are inaccurate. Insulin is often used in the management of type 2 diabetes. The condition is increasingly diagnosed in young people. Statistics Almost one in 20 Australians, or one million people, were diagnosed with type 2 diabetes mellitus in 2008. The actual proportion of Australians with the condition may be higher as many people are not diagnosed until they develop complications, for example diabetic retinopathy. Of those who have been diagnosed Continue reading >>
- Women in India with Gestational Diabetes Mellitus Strategy (WINGS): Methodology and development of model of care for gestational diabetes mellitus (WINGS 4)
- 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
- Metabolic surgery for treating type 2 diabetes mellitus: Now supported by the world's leading diabetes organizations
Type 2 Diabetes
The pancreas lies at the back of the abdomen behind the stomach and has two main functions: to produce juices that flow into the digestive system to help us digest food to produce the hormone called insulin. Insulin is the key hormone that controls the flow of glucose (sugar) in and out of the cells of the body. Type 2 diabetes is caused by: insufficient production of insulin in the pancreas a resistance to the action of insulin in the body's cells – especially in muscle, fat and liver cells. Type 2 diabetes is strongly associated with being overweight, but it's less clear what causes it, compared to the Type 1 disease. Term watch Type 2 diabetes used to be called 'non-insulin dependent diabetes'. This is because insulin injections were not part of its treatment. As some people with Type 2 also now require insulin, the term Type 2 is preferred. In the first few years after diagnosis with Type 2 diabetes high levels of insulin circulate in the blood because the pancreas can still produce the hormone. Eventually insulin production dwindles. For reasons we don't understand, the effect of insulin is also impaired. This means it doesn't have its normal effect on the cells of the body. This is called insulin resistance. What is insulin resistance? Insulin resistance has a number of knock-on effects: it causes high blood glucose it disturbs the fat levels in the blood, making the arteries of the heart more likely to clog (coronary heart disease) The insulin-producing cells of the pancreas in people with Type 2 diabetes don't seem to come under attack from the immune system as they do in Type 1. But they are still unable to cope with the need to produce a surge of insulin after a meal. Normally, this insulin surge causes the body to store excess glucose coming in and so keeps Continue reading >>
The Effect Of Short Term Intensive Insulin Therapy In Non-insulin-dependent Diabetics Who Had Failed On Sulphonylurea Therapy.
Abstract To determine the effect of short term intensive insulin therapy in non-insulin-dependent diabetes mellitus (NIDDM) we studied 10 patients who had been on maximal doses of sulphonylurea therapy, with a glycosylated haemoglobin value persistently above the normal range. All patients were non-ketonuric, had negative islet cell antibodies, and had been on sulphonylureas for a mean duration of 5.6 yr. Patients were maintained at euglycaemia (plasma glucose 4-7 mmol/l) for 24 hr using an open-loop intravenous insulin regimen, and then underwent a standard 75 g oral glucose tolerance test (OGTT). This was repeated after 3 months of treatment with insulin. Mean fasting plasma glucose and glycosylated haemoglobin were 10.1 mmol/l and 12.2% respectively before, and 7.1 mmol/l (p less than 0.001) and 8.4% (p less than 0.001) after treatment. There was no significant change in body weight. Plasma insulin and C-peptide responses to 75 g OGTT did not change significantly, but the total amount of intravenously infused insulin required for 24-hr euglycaemia fell from a mean value of 138 u before treatment to 87 u (p less than 0.001) at the end of insulin therapy. Remission, with glycosylated haemoglobin in the normal range for more than 3 months after stopping insulin, was observed in 5 out of the 10 patients. All 5 who failed to achieve remission had markedly blunted maximal insulin responses of less than 10 mu/l on both OGTT's. Our study shows that insulin treatment in NIDDM appears to exercise a beneficial effect by lowering insulin resistance. We suggest that this may be of advantage early on in patients with NIDDM in preserving B-cell reserve. Continue reading >>
- Bariatric Surgery versus Intensive Medical Therapy for Diabetes — 5-Year Outcomes
- 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)
- NIHR Signal Insulin pumps not much better than multiple injections for intensive control of type 1 diabetes
Medical Definition Of Non-insulin-dependent Diabetes
Amputations. INVOKANA® may increase your risk of lower-limb amputations. Amputations mainly involve removal of the toe or part of the foot; however, amputations involving the leg, below and above the knee, have also occurred. Some people had more than one amputation, some on both sides of the body. You may be at a higher risk of lower-limb amputation if you: have a history of amputation, have heart disease or are at risk for heart disease, have had blocked or narrowed blood vessels (usually in leg), have damage to the nerves (neuropathy) in the leg, or have had diabetic foot ulcers or sores. Call your doctor right away if you have new pain or tenderness, any sores, ulcers, or infections in your leg or foot. Your doctor may decide to stop your INVOKANA®. Talk to your doctor about proper foot care Dehydration. INVOKANA® can cause some people to become dehydrated (the loss of too much body water), which may cause you to feel dizzy, faint, lightheaded, or weak, especially when you stand up (orthostatic hypotension). You may be at higher risk of dehydration if you have low blood pressure, take medicines to lower your blood pressure (including diuretics [water pills]), are on a low sodium (salt) diet, have kidney problems, or are 65 years of age or older Yeast infection of the penis (balanitis or balanoposthitis). Men who take INVOKANA® may get a yeast infection of the skin around the penis. Symptoms include: redness, itching, or swelling of the penis; rash of the penis; foul-smelling discharge from the penis; or pain in the skin around penis Before you take INVOKANA®, tell your doctor if you have a history of amputation; heart disease or are at risk for heart disease; blocked or narrowed blood vessels (usually in leg); damage to the nerves (neuropathy) of your leg; diab Continue reading >>
Early-onset Type 2 (non-insulin-dependent) Diabetes Mellitus Is Associated With Glucokinase Locus, But Not With Adenosine Deaminase Locus, In The Japanese Population
Abstract To investigate the possible contribution of glucokinase (GCK) and adenosine deaminase (ADA) loci to the genetic susceptibility to type 2 (non-insulin-dependent) diabetes mellitus, we studied the association of these loci with type 2 diabetes in the Japanese population. Fifty patients with type 2 diabetes and 50 control subjects were analyzed for microsatellite polymorphism 3′ to the GCK gene and PstI polymorphism in the ADA gene by polymerase chain reaction. The frequency of the most common GCK allele (Z) was significantly lower in type 2 diabetic patients than that in control subjects and a longer Z + 2 allele was more common in type 2 diabetic patients (26% vs. 15%, P = 0.053), particularly in those with younger age of onset (33% vs. 15%, younger onset type 2 diabetes vs. control, P = 0.014). The frequency of genotypes containing at least one Z + 2 allele was significantly more common in type 2 diabetic patients (46% vs. 28%, P < 0.05), particularly in those with younger age of onset (61% vs. 28%, relative risk 4.00, P < 0.01). In contrast, there was no difference in allelic or genotypic frequencies of PstI polymorphism in the ADA gene between the two groups. Despite the association between the GCK locus and type 2 diabetes, none of the patients had known mutations (Glu265 → AM265, Glu279 → AM279, Gly299 → Arg299, Glu300 → Gln300, Leu309 → Pro309). These results suggest that the GCK locus, but not the ADA locus, contributes to the genetic susceptibility to type 2 diabetes in Japanese. The low frequencies of known GCK mutations shown in this and other studies suggest that the association of the GCK locus with type 2 diabetes observed in this study is due to the presence of an unknown common mutation in exons or a mutation in the regulatory region o Continue reading >>
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Objective: To determine whether insulin-requiring patients with non-insulin-dependent diabetes mellitus (NIDDM) and good glycemic control would benefit in weight control, serum lipid concentrations, or blood pressure from a reduction in exogenous insulin treatment. Methods: Eighteen patients with well-controlled NIDDM who required insulin therapy were entered into a randomized, placebo-controlled, double-blind, crossover study of the addition for 12 weeks of treatment with a second-generation sulfonylurea agent (micronized glyburide). Results: The mean fasting plasma glucose at entry was 7.00 - 0.22 mmol/L and at the end of the 12-week treatment phase was 7.67 - 0.39 mmol/L with placebo and 7.28 - 0.44 mmol/L with active drug. Hemoglobin A1c was unchanged during the study (7.5 - 0.2% at entry, 7.5 - 0.3% with placebo, and 7.4 - 0.3% with active drug). Addition of the orally administered agent resulted in a 29% decrease in exogenous insulin requirements and a 37% increase in 24-hour urinary C-peptide excretion. Patients had no change in weight after 12 weeks of either placebo or active drug. Plasma cholesterol levels declined slightly during the study, but they did not differ significantly during drug and placebo treatment. Blood pressure was unchanged in both the subjects with and without hypertension. Conclusion: In patients with NIDDM and good glycemic control with insulin treatment, a glyburide-related increase in endogenous insulin secretion caused a proportionate decrease in exogenous insulin requirements. With continued good glycemic control, however, the orally administered agent showed no additional benefit on weight, blood pressure, plasma triglycerides, or low-density lipoprotein or high-density lipoprotein cholesterol. Continue reading >>
Type 2 Diabetes - Non-insulin Dependent - Low Risk Of Hypoglycaemia
See also: Definition This guidance should be used for applicants treated with any of: Diet Acarbose Metformin Gliptens (GPP-4 inhibitors) Exenatide (GLP-1 agonists) Aeromedical Implications Effect of aviation on condition Irregular meal and sleep times Sedentary occupation Effect of condition on aviation Overt incapacitation Cardiovascular event Cerebrovascular event Subtle incapacitation - end-organ damage Visual impairment (fields, low contrast sensitivity, colour) Impaired motor and sensory nerve function Impaired autonomic function (hypoglycaemia awareness) Effect of treatment on aviation Side-effects including GI and pancreatitis Approach to medical certification Most information required for assessments is already undertaken as part of best-practice management guidelines. See Diabetes Australia and RACGP for guidance. Based on the condition Confirmed diagnosis Complications of diabetes (eye, heart, brain, kidney) Absence of autonomic neuropathy Based on Treatment Absence of significant side effects Demonstrated Stability HbA1c less than 7.5% Risk assessment protocol - Information required New cases Treating doctor report (GP or Endocrinologist) detailing: Current status of diabetes Assessment of control, HbA1c Evidence of end-organ damage (eyes, heart, kidneys, brain, erectile dysfunction) Treatment A report from an Ophthalmologist or Optometrist detailing: Visual acuity (with and without correction) Retinal disease Pressures (and treatment if required) Any other ophthalmic pathology (fields / contrast sensitivity / colour vision) An assessment by the DAME of the cardiac risk index. IF more than 14, a report from a Cardiologist with respect to: any confirmed diagnosis clinical status including any symptoms investigations conducted including the results of a recent Continue reading >>
Diabetes: Differences Between Type 1 And 2 - Topic Overview
In general, people with diabetes either have a total lack of insulin (type 1 diabetes) or they have too little insulin or cannot use insulin effectively (type 2 diabetes). Type 1 diabetes (formerly called juvenile-onset or insulin-dependent diabetes), accounts for 5 to 10 out of 100 people who have diabetes. In type 1 diabetes, the body's immune system destroys the cells that release insulin, eventually eliminating insulin production from the body. Without insulin, cells cannot absorb sugar (glucose), which they need to produce energy. Type 2 diabetes (formerly called adult-onset or non-insulin-dependent diabetes) can develop at any age. It most commonly becomes apparent during adulthood. But type 2 diabetes in children is rising. Type 2 diabetes accounts for the vast majority of people who have diabetes-90 to 95 out of 100 people. In type 2 diabetes, the body isn't able to use insulin the right way. This is called insulin resistance. As type 2 diabetes gets worse, the pancreas may make less and less insulin. This is called insulin deficiency. How are these diseases different? Differences between type 1 and type 2 diabetes Type 1 diabetes Type 2 diabetes Symptoms usually start in childhood or young adulthood. People often seek medical help, because they are seriously ill from sudden symptoms of high blood sugar. The person may not have symptoms before diagnosis. Usually the disease is discovered in adulthood, but an increasing number of children are being diagnosed with the disease. Episodes of low blood sugar level (hypoglycemia) are common. There are no episodes of low blood sugar level, unless the person is taking insulin or certain diabetes medicines. It cannot be prevented. It can be prevented or delayed with a healthy lifestyle, including maintaining a healthy wei Continue reading >>
Fasting Hyperglycemia In Non-insulin-dependent Diabetes Mellitus: Contributions Of Excessive Hepatic Glucose Production And Impaired Tissue Glucose Uptake☆
Abstract The factors responsible for fasting hyperglycemia were investigated in 77 normal weight non-insulin-dependent diabetic (NIDD) and 72 age-, sex-, and weight-matched control individuals. In diabetic subjects with mild fasting hyperglycemia (<140 mg/dL) hepatic glucose production (1.85 ± 0.03 mg/kg · min) was similar to controls (1.84 ± 0.02); the major factor responsible for the elevated basal glucose level in the diabetic group was a decreased efficiency in the tissue uptake of glucose, as reflected by a 30% decline in the rate of glucose clearance (1.56 ± 0.03 v 2.00 ± 0.03 mL/kg · min, P < .001). In contrast, in diabetic subjects with fasting plasma glucose concentrations above 140 mg/dL, basal hepatic glucose production was significantly elevated (2.42 ± 0.08 mg/kg · min, P < .001) and correlated closely with the increase in fasting plasma glucose concentration (r = .796, P < .001). The basal rate of whole body glucose clearance reached a plateau value at fasting glucose levels of 160 to 180 mg/dL and did not contribute to the further rise in fasting plasma glucose concentrations above 160 to 180 mg/dL. Decreased efficiency of tissue glucose uptake is responsible the development of fasting hyperglycemia in patients with mild NIDDM (fasting plasma glucose < 140 mg/dL). As the diabetic state worsens, an increase in basal hepatic glucose production is the major factor responsible for the progressive rise in fasting glucose levels. Continue reading >>
- Excessive fruit consumption during the second trimester is associated with increased likelihood of gestational diabetes mellitus: a prospective study
- 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
- Antidepressant Medication as a Risk Factor for Type 2 Diabetes and Impaired Glucose Regulation
Non-insulin Dependent Diabetes (insulin Therapy In)
the United Kingdom Prospective Diabetes Study Group (UKPDS) has pointed out that majority of type 2 diabetes patients will experience progressive pancreatic beta cell dysfunction even when their diabetes control is excellent (1) so type 2 diabetics may eventually require treatment with insulin when oral hypoglycaemic medication is no longer effective a straight swap to insulin treatment is usual if the maximal therapy with non-insulin treatments have been reached according to estimations in UK general practice, only 50% of patients who require insulin due to failure of oral medication will receive it within 5 years o the average time taken from beginning treatment with the last oral agent to beginning insulin therapy is around 8 years (2) in the case of overweight patients taking metformin, then treatment with metformin may be continued - this is because metformin may attenuate weight gain resulting from the introduction of insulin therapy insulin therapy and a sulphonylurea may decrease the amount of insulin actually required and enhance the use of a single night-time dose but overall the clinical advantages of this combination are small (3) the average weight gain resulting from introduction of insulin therapy is 4 kg - however some patients may have a marked increase in weight after onset of insulin therapy in a comprehensive review of combination therapies with insulin in type 2 diabetes Yki-Jarvinen suggests an algorithm for starting insulin in an insulin naive type 2 diabetic patient who is on maximal oral hypoglycaemic therapy. In this algorithm she suggests stopping sulphonylurea treatment and continuation of metformin at a dose of 2g per day in combination with insulin treatment (4). If the patient is not on a dose of 2g per day when conversion to insulin occur Continue reading >>
