Leptin May Play Role in Preventing Type II Diabetes

The hormone leptin, regarded as a potential source of new fat-fighting drugs, may also be able to play a role in preventing a form of diabetes, scientists say. In a report in edition of Proceedings of the National Academy of Sciences, researchers at the University of Texas Southwestern Medical Center in Dallas said leptin may be able to prevent type II diabetes (noninsulin-dependent diabetes mellitus). Obesity can contribute to that form of the disease. The new research was based on studies of rats, and there was uncertainty among scientists about whether the hormone worked the same way in humans. The Texas researchers found that leptin receptors work in several organs, including the pancreas, the source of insulin. Earlier studies focused on how leptin works in the brain to control appetite.

"Our findings show for the first time that if you take tissue out of the body and put it in a little culture dish, where there is obviously is no central nervous system, then add leptin, you will find that leptin has a direct effect on fat degradation," Michio Shimabukuro, a scientist at Southwestern, said.

The study linked defective leptin receptors to obesity, which in turn prevented insulin from correctly controlling glucose, which is a large part of what goes wrong in type II diabetes.

diabetes mellitus - general information

Diabetes Mellitus,mostly called Diabetes, is a serious disease, but however if proper care is taken is not fatal. There are three types ofdiabetes: Type I, Type II, and Gestational diabetes. Even though the are all different types of diabetes they are all very different, but everyone with diabetes has one thing in common: Their bodies have extremely limited, if any ability to move sugar, or glucose, to their cells, and glucose is the most important and primary fuel of the body.

All humans require the use of glucouse, because of the simple reason that it powers the entire body. Glucose is actually a very simple type ofsugar, actually it is the simplest for of sugar, and it powers all cells throughout the body.

People who do not have diabetes rely on the insulin created by the body. Insulin is a hormone that is used for the purpose of moving glucose from the blood into the body's cells. But people who have diabetes either don't produce insulin or cannot use the insulin they produce. Without insulin, the cells cannot move glucose into the cells. Glucose gathers in the blood, this alone is called hyperglycemia, which is the scientific term for too much glucose in blood, hyper meaning too much and glycemia meaning glucose incells. The symptoms of hyperglycemia include incredible thirst, the need to urinate frequently, unclear or blurry vision,nasea and fatigue, and much more. Hyperglycemia is not a disease that happens over night, because over time high blood glucose can cause serious medical problems

Aspirin therapy in diabetes.

What Are The Recommendations For Regular Aspirin Therapy in People With Diabetes?
People with diabetes have an increased risk of dying from the complications of cardiovascular disease, especially atherosclerosis and vascular thrombosis. Platelets contribute to the development of these disorders. A major mechanism underlying the activity of platelets involves the increased production of thromboxane, a potent vasoconstrictor. Since aspirin blocks thromboxane synthesis, its use as a primary and secondary strategy to prevent cardiovascular disease has been supported. Indeed, studies have shown that daily low-dose aspirin therapy reduces the risk of cardiovascular disease in patients with diabetes.

This position statement outlines the recommendations for regular aspirin therapy in people with diabetes. These recommendations include the following:

1. Use aspirin therapy as a secondary prevention strategy in diabetic men and women with evidence of large vessel disease. This includes diabetic men and women with a history of myocardial infarction, vascular bypass procedure, stroke or transient ischemic attack, peripheral vascular disease, claudication, and/or angina.

2. In addition to treating the primary cardiovascular risk factor(s) identified, consider aspirin therapy as a primary prevention strategy in high-risk men and women with type 1 or type 2 diabetes. This includes diabetic patients with the following:
* a family history of coronary artery disease
* cigarette smoking
* hypertension
* obesity (>120% desirable weight); BMI >28 in women, >27.3 in men
* albuminuria (micro or macro)
* lipids: cholesterol >200 mg/dL; LDL-cholesterol >130 mg/dL; HDL-cholesterol <40>250 mg/dL

3. The following individuals may not be candidates for aspirin therapy:
* diabetic individuals under age 30 years without the cardiovascular risk factors listed above
* people with aspirin allergy (ticlopidine may be considered as an aspirin substitute), bleeding tendency, anticoagulant therapy, recent gastrointestinal bleeding, and clinically active hepatic disease

4. Dosage: Use enteric-coated aspirin in doses of 81-325 mg/day.

Ref: Diabetes Care.

Blood Pressure Pill Helps Prevent Diabetes

A drug used to control high blood pressure appears to help prevent diabetes in high-risk people, a study indicates.

The drug is ramipril, marketed as Altace. It is an ACE inhibitor, a member of a class of drugs most often prescribed to prevent heart disease. Its diabetes connection emerged from a study intended to measure its effect on the incidence of heart disease.

Ramipril reduced the risk of diabetes by about 40 percent in that trial, which included persons at high risk of heart attack and stroke, says a report in the latest issue of The Journal of the American Medical Association . Only 3.4 percent of the people in that trial who took ramipril developed diabetes, compared with 5.6 percent of those who got a placebo.

That result requires confirmation, says study leader Salim Yusuf, professor of medicine at McMaster University in Hamilton, Ontario. That study was not intended to measure the effect of the drug on diabetes, he says. A multicenter trial will be undertaken "because of the enormous clinical and public health implications of these findings," Yusuf says.

Ramipril is the second drug shown to have promise in preventing diabetes, says Dr. Eugene Barrett, director of the diabetes center at the University of Virginia. The other is metformin, marketed as Glucophage, which is used to reduce blood levels of glucose in diabetics.

Yusuf say his study showed that ramipril also reduces blood sugar levels.

Barrett says, "It was a surprise that ramipril has an effect on blood glucose. Now this finding has to be confirmed."

Barrett says besides the two drugs, the good news is that simple lifestyle changes can prevent diabetes in high-risk individuals. "Modest exercise and fairly modest dietary restrictions can prevent diabetes in that population," he says.

The recommendations for exercise and diet to prevent diabetes are generally the same as those to prevent heart disease, including a diet low in fat and high in fruits and vegetables, and at least 30 minutes of physical activity, such as a brisk walk, every day.

People at high risk for diabetes include those who are overweight and who have a family history of the disease. African-Americans, Hispanics and women who have diabetes during pregnancy also are at high risk, Barrett says.

The incidence of diabetes has been rising in recent years, largely because Americans are gaining more weight and getting less physical activity. The Centers for Disease Control and Prevention (CDC) reported earlier this year that the incidence of diabetes increased by a third from 1990 to 1998, from 4.9 percent to 6.5 percent of the adult American population. The CDC say 800,000 new cases of diabetes are reported each year.

Now there is hope of reversing that trend, Barrett says. "People can watch their diet and exercise, and now at least two pharmacological agents look promising," he says.

Treating Foot Infections in Diabetics

The Best Approach to Treating Foot Infections in Diabetics
Foot infections occur in about one quarter of diabetics and are among the most common causes of hospitalization of diabetic patients. More than 50,000 lower-extremity amputations are performed each year, and a substantial number result from the failure to treat infected feet. Clinical findings, bone biopsies, and imaging studies (roentgenograms, bone scans, white blood cell scans, and magnetic resonance imaging) are used to evaluate patients with foot infections, but it is still difficult to tell superficial soft- tissue infections from chronic osteopathy or osteomyelitis.
Recently Eckman et al. reviewed the literature to determine which diagnostic approach is the most cost-effective, while still providing adequate care. They compared the outcomes of various forms of intervention following surgical debridement and intravenous antibiotic therapy:

a short course of antibiotics for presumed soft-tissue infection;
culture-guided empiric treatment with a long course of antibiotics for presumed osteomyelitis;
71 combinations of diagnostic tests (including radiographs, scans, imaging, and biopsies) preceding antibiotic therapy for osteomyelitis;
71 combinations of diagnostic tests preceding amputation; and immediate amputation.
The main outcome measures were quality-adjusted life expectancy and average costs.
The investigators found that culture-guided empiric treatment for osteomyelitis with 10 weeks of oral antibiotic therapy was similar in efficacy, and far less costly, than diagnostic testing followed by antibiotic therapy. Radiographs, scans, magnetic resonance imaging, and biopsies add considerable expense to the treatment of patients with suspected osteomyelitis of the foot -- probably as much as $100 million annually -- yet such testing may result in little improvement in health outcomes. Imaging studies lack precision, and biopsies are too easily contaminated by overlying soft tissue infection.

"Since safe, convenient and effective oral antibiotic regimens are available, there is little to be gained by testing," said the investigators. The only caveat is that vascular perfusion must be assessed; inadequate perfusion can have a negative affect on the outcome of antibiotic therapy. The investigators concluded, "In patients who show no signs of systemic infection and who have adequate perfusion, surgical debridement followed by a 10-week course of culture-guided oral antibiotics may be as effective as and less costly than other approaches."

Eckman MH et al. JAMA

Age and diabetes risk

IDDM can develop at any age, although onset is more common at puberty. There is another (small) peak during midlife. More cases occur during late fall or early winter than any other season, wrote Atkinson and Maclaren. Susceptibility is inherited; the primary gene associated with IDDM is the major histocompatibility complex on chromosome 6, a region associated with genes for the immune system recognition molecules referred to as HLA. In the United States, IDDM is 20 times as common in white persons with HLA types DR3 and DR4 as in the general population. Another gene for IDDM susceptibility has been found on chromosome 11 near the genes for insulin and insulin- like growth factor. There are also 20 other chromosomal regions associated with IDDM predisposition. IDDM is about three times as likely to develop in children whose fathers have IDDM as in those whose mothers have the disease. Not all persons with a genetic susceptibility get the disease: among identical twins, one twin may have IDDM and the other not. The viral model of IDDM explains this discordance; exposure to the pathogen is necessary for triggering the autoimmune attack, and not all persons will "catch" a virus, even when exposed to infected family members.
Atkinson MA, Maclaren NK. N Engl J Med.

insulin and diabtes mellitus

Diabetes is one of the major causes of physician visits, and the fourth leading cause of death in the US. Direct and indirect costs of diabetes and its complications are estimated at $100 billion annually, amounting to approximately 12% of the total annual US health care expenditure. There are two distinct types of diabetes: insulin-dependent diabetes mellitus (IDDM), also called Type 1 or juvenile diabetes; and non-insulin-dependent diabetes mellitus (NIDDM), also called Type II or adult-onset diabetes. IDDM occurs when the immune system attacks and destroys the pancreatic insulin-producing cells, while NIDDM occurs when cells in the body lose the ability to respond efficiently to insulin, a condition termed "insulin resistance."

In both IDDM and NIDDM, the hyperglycemia results in the excretion of glucose in the urine (which causes an increase in urine production) and the increased release of fatty acids from adipose tissue, with resulting increased ketone production by the liver. The accumulation of ketone bodies can cause life-threatening ketoacidosis. NIDDM patients, particularly elderly patients with underlying illnesses, may also develop another life-threatening condition--nonketotic hyperosmolar state--characterized by extremely high blood sugar levels. While these severe hyperglycemic episodes can be life-threatening, chronic hyperglycemia is also a cause of premature death in diabetics. Hyperglycemia and associated metabolic abnormalities--the production of advanced glycation end products, intracellular accumulation of sorbitol, and dyslipidemias--lead to complications such as retinopathy, renal damage, peripheral neuropathy, hypertension, cerebral, peripheral, and coronary artery disease, and neuroischemic gangrene requiring amputation. Managing IDDM requires 1-4 daily injections of insulin, plus careful planning of diet and exercise. NIDDM is managed with diet, exercise, weight loss, oral hypoglycemics, and insulin when necessary. And patients with both types of diabetes must guard against the complications.

Rubenstein AH. JAMA.

Insulin-dependent Diabetes and beta cells

IDDM is an autoimmune disease in which the body attacks and ultimately destroys the beta-cells. While the classic symptoms-- hyperglycemia and ketosis--can develop rapidly, the disease itself is a chronic process that may be present for years. Symptoms occur late in the course of the disease, after most of the beta-cells have been destroyed. Autoantibodies against islet-cell components or insulin have been found in at-risk patients years before clinical diabetes developed. In a comprehensive review of IDDM, Atkinson and Maclaren wrote that the autoimmune attack is probably triggered by a virus whose proteins share an amino acid sequence with a beta-cell protein. One candidate is Coxsackie virus, which causes a systemic infection. It is also possible that a virus may infect beta-cells directly, causing cell death and sensitization of the immune system to beta-cell components. It was suggested recently that drinking cow's milk in early life may initiate beta-cell destruction through molecular mimicry, but subsequent studies have not turned up much supporting evidence.
source:Atkinson MA, Maclaren NK. N Engl J Med.

Diabetes Mellitus: Insulin-dependent and Non-insulin-dependent

Diabetes mellitus is a fairly common metabolic disease characterized by hyperglycemia due to the loss of insulin-secreting beta-cells in the pancreatic islets of Langerhans. The disease and its devastating complications cost Americans about $50 billion annually. There are two distinct forms of diabetes, termed insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The first is an autoimmune disease; the second is associated with insulin resistance. Both have a genetic component. In the United States, the lifetime prevalence of IDDM is 0.4%, and that of NIDDM about 7%.