Information

Is diabetes mellitus a sex-linked disease?

Is diabetes mellitus a sex-linked disease?


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

There are two types of diabetes mellitus.

a. Type 1 diabetes mellitus b. Type 2 diabetes melliuts

Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?


Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

Neither are sex-linked. Type 1 can be directly inherited (in a non-Mendelian fashion), but Type 2 genetic factors mostly increase risks. "Recessive genetic traits" are traits that only express themselves when ONLY the recessive alleles are present in the organism (a dominant allele, if present, will 'overpower' recessive one).

Longer info:

Diabetes mellitus Type 1 (Juvenile Diabetes) is inherited, but it is autosomal with complex dominant/recessive rules:

Type 1 diabetes is a polygenic disease, meaning many different genes contribute to its onset. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between.

That results in some interesting, albeit complex, expressions:

The risk of a child developing type 1 diabetes is about 10% if the father has it, about 10% if a sibling has it, about 4% if the mother has type 1 diabetes and was aged 25 or younger when the child was born, and about 1% if the mother was over 25 years old when the child was born.

Diabetes mellitus Type 2 does have genetic components, but the vast majority merely increase the risk of developing Type 2 Diabetes. Environmental factors play a large role in Type 2.

Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.


What is Diabetes?

With diabetes, your body either doesn&rsquot make enough insulin or can&rsquot use it as well as it should.

Diabetes is a chronic (long-lasting) health condition that affects how your body turns food into energy.

Most of the food you eat is broken down into sugar (also called glucose) and released into your bloodstream. When your blood sugar goes up, it signals your pancreas to release insulin. Insulin acts like a key to let the blood sugar into your body&rsquos cells for use as energy.

If you have diabetes, your body either doesn&rsquot make enough insulin or can&rsquot use the insulin it makes as well as it should. When there isn&rsquot enough insulin or cells stop responding to insulin, too much blood sugar stays in your bloodstream. Over time, that can cause serious health problems, such as heart disease, vision loss, and kidney disease.

There isn&rsquot a cure yet for diabetes, but losing weight, eating healthy food, and being active can really help. Taking medicine as needed, getting diabetes self-management education and support, and keeping health care appointments can also reduce the impact of diabetes on your life.

  • 34.2 million US adults have diabetes, and 1 in 5 of them don&rsquot know they have it.
  • Diabetes is the seventh leading cause of death in the United States.
  • Diabetes is the No. 1 cause of kidney failure, lower-limb amputations, and adult blindness.
  • In the last 20 years, the number of adults diagnosed with diabetes has more than doubled.

Diabetes Mellitus

Giovanni Davì , . Natale Vazzana , in Platelets (Third Edition) , 2013

I Accelerated Atherothrombosis: Epidemiological and Clinical Findings

Diabetes mellitus (DM) is a strong predictor of cardiovascular morbidity and mortality and is associated with both micro- and macrovascular complications. 1 Cardiovascular disease (CVD) causes up to 70% of all deaths in people with DM. The epidemic of DM will thus be followed by a burden of diabetes-related vascular diseases. The number of DM patients increases with aging of the population, in part because of the increasing prevalence of obesity and sedentary lifestyle. Although the mortality from coronary artery disease (CAD) in patients without DM has declined since the 1990s, the mortality in men with type 2 diabetes (T2DM) has not changed significantly. 2 Moreover, DM is an independent risk factor for heart failure. Heart failure is closely related to diabetic cardiomyopathy: changes in the structure and function of the myocardium are not directly linked to CAD or hypertension. Diabetic cardiomyopathy is clinically characterized by an initial increase in left ventricular stiffness and subclinical diastolic dysfunction, gradually compromising left ventricular systolic function with loss of contractile function and progress into overt congestive heart failure. DM accounts for a significant percentage of patients with a diagnosis of heart failure in epidemiologic studies such as the Framingham Study and the UK Prospective Diabetes Study (UKPDS). 2 A 1% increase in glycated hemoglobin (HbA1c) correlates to an increment of 8% in heart failure. 3 The prevalence of heart failure in elderly diabetic patients is up to 30%. 3

Accelerated atherosclerosis is the main underlying factor contributing to the high risk of atherothrombotic events in DM patients. CAD, peripheral vascular disease, stroke, and increased intima-media thickness are the main macrovascular complications. Diabetics are 2–4 times more likely to develop stroke than people without DM. 2 CVD, particularly CAD, is the leading cause of morbidity and mortality in patients with DM. 4 Patients with T2DM have a 2- to 4-fold increase in the risk of CAD, and patients with DM but without previous myocardial infarction (MI) carry the same level of risk for subsequent acute coronary events as nondiabetic patients with previous MI. 5 Furthermore, people with diabetes have a poorer long-term prognosis after MI, including an increased risk for congestive heart failure and death.

DM is a strong independent predictor of short- and long-term recurrent ischemic events, including mortality, in acute coronary syndrome (ACS), 6,7 including unstable angina and non-ST-elevation MI (NSTEMI), 8 ST-elevation MI (STEMI) treated medically, 9 and ACS undergoing percutaneous coronary intervention (PCI). 10,11 Furthermore, the concomitant presence of cardiovascular risk factors and comorbidities that negatively affect the outcomes of ACS is higher in DM patients. 12


4. Relation between the Pathological Features Exhibited in Hyperthyroidism and T2DM: Role of Insulin Resistance and Other Factors

The pathological features of T2DM include increased intestinal glucose absorption, reduced insulin secretion, and change in the β-cell mass [22]. Further, symptoms also include increased insulin degradation [23], increased glucagon secretion [24], increased hepatic glucose production [24], enhanced catecholamines, and insulin resistance [25]. These factors have been investigated to be an integral part of hyperthyroidism as well [26]. Hence, an intersection of pathological basis occurs which gives us cue to an array of physiological aberrations which are common in hyperthyroidism and T2DM. Among the above-mentioned symptomatology, insulin resistance has been the most important facet connecting thyroid dysfunction and T2DM. Insulin resistance is a condition which occurs in both hypothyroidism and hyperthyroidism [27].

Insulin resistance in the muscles and liver is a characteristic feature of T2DM. An undisturbed glucose homeostasis and intact insulin secretary response and unperturbed sensitivity of the tissues to insulin are essential to maintain normal blood glucose levels [28�].

Glucose disposal is mediated by the conjoint effect of insulin and hyperglycemia to modulate three basic phenomenon. Firstly, diminution of endogeneous (hepatic) glucose production. Secondarily, enhanced uptake of glucose (hepatic and splanchnic). Thirdly, upregulation of glucose by peripheral tissues (skeletal muscles). Glucose uptake into muscles is modulated by glycolysis and glycogen synthesis. Hepatic insulin resistance is characterized by glucose overproduction inspite of fasting hyperinsulinemia, and enhanced rate of hepatic glucose output was the pivotal modulator of increased fasting plasma glucose (FPG) concentration in T2DM subjects [24]. In insulin resistance in the postabsorptive state, muscle glucose is upregulated but the efficiency of uptake is reduced. In the wake of such conditions, reduced glucose uptake into the muscles and enhanced hepatic glucose output lead to worsening of glucose metabolism.

The term harmonious quartet is used to address the core pathology of insulin resistance [24]. Deregulated glucose disposal and metabolism in adipocytes, muscles, and liver, along with impaired insulin secretion by the pancreatic beta cells, constitute the four major organ system abnormalities which play a definitive role in the pathogenesis of T2DM. It is worth considering that insulin resistance has been a proven condition in hyperthyroidism as well as hypothyroidism. Insulin resistance also leads to impaired lipid metabolism according to recent findings [32]. Hence, it appears that insulin resistance is the possible link between T2DM and thyroid dysfunction.

Insulin resistance and β cell function are inversely correlated with thyroid stimulating hormone which may be explained by insulin-antagonistic effects of thyroid hormones along with an increase in TSH. The higher serum TSH usually corresponds to lower thyroid hormones via negative feedback mechanism. As TSH increased, thyroid hormones decreased and insulin antagonistic effects are weakened. These observations demonstrate that insulin imbalance is closely associated with thyroid dysfunction and the phenomenon id mediated via β cell dysfunction [33].

4.1. Association of Insulin Resistance in Hyperthyroidism and Subclinical Hyperthyroidism

Hyperthyroidism has been associated with insulin resistance which has been linked with elevated glucose turnover, increased intestinal glucose absorption, elevated hepatic glucose output, increased free fatty acid concentrations, increased fasting and or postprandial insulin an proinsulin levels, and increased peripheral glucose transport accompanied by glucose utilization [27, 34]. T2DM patients with thyroid dysfunction have been proven to be more susceptible to ketosis [35] and ketogenesis [36]. Insulin resistance has been shown to be associated with subclinical hypothyroidism, which is in turn linked to impaired lipid balance and risk of development of metabolic syndrome [37�].

4.1.1. Role of Liver

In hyperthyroidism, endogenous glucose production is elevated and reduces hepatic insulin sensitivity in humans [40] due to glycogenesis and glycogenolysis. The role of hypothalamus mediated sympathetic action in liver has been proposed [41] along with increased expression of GLUT 2 transporters in liver which ultimately lead to elevation in plasma free fatty acid [42, 43].

4.1.2. Role of Muscles

There is marked increase in the skeletal glucose utilization in hyperthyroid state [34]. Increased glucose utilization has been reported to be mediated by insulin stimulated glucose oxidation rates [44�]. Under such conditions, reduced glyco genesis has been reported due to insulin stimulated nonoxidative glucose disposal, which is accompanied by redirection of intracellular glucose towards glycolysis and lactate formation [27]. The transport of lactate from periphery to liver leads to enhanced production of glucose via Cori's cycle. Hyperthyroidism has also been associated with enhanced insulin sensitivity [47]. Increased peripheral insulin resistance has been coupled with elevated expression of bioactive inflammatory mediators including adipokines (IL-6 and TNF-alpha) [16] which lead to insulin resistance.

4.1.3. Role of Fat Tissues

Haluzik et al. summarized that rate of local lipolysis in the abdominal subcutaneous adipose tissue was a result of modulation of norepinephrine (NE) levels and adrenergic postreceptor signaling by thyroid hormones [48]. Other studies reported that thyroid hormones are necessary for the mobilization of the tissue lipids especially brown adipose tissues (BATs) which are the fuel for the production of heat [49]. Hypothyroidism and decreased thyroid hormone level are responsible for decreased thermogenesis in BAT. S14 and lipogenesis are important factors for thermogenesis mediated by thyroid hormone [50].

4.2. Association of Insulin Resistance in Hypothyroidism and Subclinical Hypothyroidism

Insulin resistance has been shown to be caused in hypothyroidism in various in vitro and preclinical studies [51�] where it was found that peripheral muscles became less responsive in hypothyroid conditions. A possible role of dysregulated metabolism of leptin has been implicated for such pathology [53]. A direct relation between hypothyroidism and insulin resistance has been demonstrated by various authors [15, 54�].

Subclinical hypothyroidism has been reported to be associated with insulin resistance [55, 57, 58]. However, conflicting findings have also been reported by other workers [59, 60], indicating the need of further investigations in this domain.


The Link Between Diabetes and Kidney Disease

People with diabetes are at high risk for kidney disease, but there are steps they can take to protect their kidneys.

Meda E. Pavkov, MD, PhD, medical epidemiologist in the Chronic Kidney Disease Initiative within the Division for Diabetes Translation at the Centers for Disease Control and Prevention (CDC), is a co-author of the “Kidney Disease in Diabetes” chapter in the NIDDK publication Diabetes in America, 3 rd Edition. Here, she discusses the link between diabetes and kidney disease and the importance of early detection and management of kidney disease.

Q: What is the link between diabetes and kidney disease?

A: Diabetes is the most frequent cause of chronic kidney disease, not only in the United States but in most industrialized countries. Kidney disease in people with diabetes is caused by multiple factors, including diabetic changes in the kidneys as well as vascular changes due to hypertension. People with diabetes have high glycemia, or blood glucose, which can damage the kidneys and lead to kidney disease.

When people are diagnosed with diabetes, they may already have hypertension. Hypertension is an additional risk factor for diabetic kidney disease because high blood pressure damages the kidneys, which may prevent proper function.

Q: What are the benefits of talking about kidney disease risk factors with patients who have diabetes?

A: Most of the risk factors for kidney disease in patients with diabetes can be modified. We can treat and manage them. However, like many other chronic diseases, kidney disease has very few early symptoms. For instance, a patient may have albuminuria, which is the earliest sign of kidney disease. It means that there is too much of the protein albumin in the urine, but a patient may not have any symptoms specific to the albuminuria.

The prevalence of kidney disease in the United States is about 15 percent, yet awareness of kidney disease is very low. Patients can have kidney disease for a long time without having symptoms or knowing that they have the disease. We found that many transplant patients and new dialysis patients had little awareness of their kidney disease and did not know what they could have done to help prevent or slow the disease before kidney failure.

It is especially important to talk to patients with diabetes about kidney disease risk factors because they are more than twice as likely to develop kidney disease than those without diabetes. By talking with patients who have diabetes about kidney disease, the disease may be diagnosed early, and patients can take steps to help slow its progression.

Q: Why is it so important to diagnose kidney disease in patients with diabetes as early as possible?

A: By diagnosing kidney disease as early as possible, we can treat the disease earlier, which means slowing disease progression. The end goal for treating kidney disease as early as possible is to prevent kidney failure, which is when the kidneys have lost most of their ability to function. By preventing kidney failure, you avoid end-stage renal disease, which is the stage at which dialysis or a kidney transplant is needed to survive.

Patients with diabetes who know they have kidney disease can

  • avoid certain medicines, such as nonsteroidal anti-inflammatory drugs, which can worsen or accelerate kidney disease progression
  • modify their diets to slow or prevent kidney disease from progressing

Diagnosing and managing kidney disease early can prevent complications, particularly cardiovascular complications. Many physicians and researchers are not aware that among people with diabetes, kidney disease doubles the risk for cardiovascular disease.

Beyond the positive health implications of diagnosing and treating kidney disease early, CDC has published studies demonstrating that diagnosing and treating the disease early to avoid kidney failure and other complications is cost effective.

Q: What are the recommended guidelines for kidney disease testing?

A: Kidney disease is diagnosed and tracked using two tests. One is a blood test, called serum creatinine, used to calculate the glomerular filtration rate (GFR), or kidney function, which assesses how well the kidneys are filtering blood. A GFR below 60 for at least 3 months indicates chronic kidney disease.

The other test used to diagnose and monitor kidney disease checks for albumin in the urine. Anyone with a urine albumin result above 30 milligrams per gram for at least two out of three albumin tests in a 3-month period is considered to have kidney disease. Physicians should be aware of the importance of the urine albumin test, because it is able to detect early kidney disease.

Guidelines recommend that anyone with one or more risk factors for kidney disease—people with diabetes, hypertension, or heart disease those with a family history of kidney disease or diabetes people older than 50 years and those who smoke—be tested for kidney disease. Testing for kidney disease is inexpensive and easy and is critical to identifying and treating the disease early.

Q: How can health care professionals help to prevent or slow kidney disease from progressing in patients with diabetes?

A: It’s important for health care professionals to educate patients about their risk for kidney disease, how the disease might affect their health, what they need to avoid, and how they can modify their lifestyle to prevent or slow the disease. When patients understand their risks, they may be more likely to talk with their health care professional about getting tested for kidney disease and more aware of the importance of keeping their kidneys healthy.

In general, kidney disease progresses relatively slowly with few or no symptoms, so there is a very long window of opportunity to personalize and adjust treatment to a patient's situation. The first and most important way to prevent or slow kidney disease in people with diabetes, whether it’s type 1 or type 2 diabetes, is to manage blood glucose levels. Glucose levels should be monitored regularly. Another way to help prevent or slow kidney disease progression is by managing blood pressure. This is particularly important in patients with type 2 diabetes, who often have high blood pressure. Lifestyle changes and medications such as ARBs, or angiotensin receptor blockers, often play a key role in controlling blood pressure in people with diabetes.

Ultimately, the best way to prevent kidney disease is to prevent type 2 diabetes, because nearly 40 percent of people with diabetes will develop kidney disease.

Q: Is there anything else that health care professionals should know about kidney disease in people with diabetes?

A: The U.S. Department of Health and Human Services recently announced an important new kidney disease initiative called Advancing American Kidney Health (PDF, 71.09 MB) . The initiative has three main goals—to reduce the number of Americans developing kidney failure, encourage home dialysis rather than treatment in dialysis centers, and increase the number of kidneys available for transplant.

This initiative is exciting because it recognizes kidney disease as an important public health issue and creates an official policy framework to improve kidney care in the United States. It aims to improve prevention and treatment, redesign dialysis to improve the quality of life among dialysis patients and increase their life expectancies, and create incentives for individuals to donate kidneys.


Prevention

Simple lifestyle measures have been shown to be effective in preventing or delaying the onset of type 2 diabetes. To help prevent type 2 diabetes and its complications, people should:

  • achieve and maintain a healthy body weight
  • be physically active &ndash doing at least 30 minutes of regular, moderate-intensity activity on most days. More activity is required for weight control
  • eat a healthy diet, avoiding sugar and saturated fats and
  • avoid tobacco use &ndash smoking increases the risk of diabetes and cardiovascular disease.

Diagnosis and treatment

Early diagnosis can be accomplished through relatively inexpensive testing of blood sugar.

Treatment of diabetes involves diet and physical activity along with lowering of blood glucose and the levels of other known risk factors that damage blood vessels. Tobacco use cessation is also important to avoid complications.

Interventions that are both cost-saving and feasible in low- and middle-income countries include:

  • blood glucose control, particularly in type 1 diabetes. People with type 1 diabetes require insulin, people with type 2 diabetes can be treated with oral medication, but may also require insulin
  • blood pressure control and
  • foot care (patient self-care by maintaining foot hygiene wearing appropriate footwear seeking professional care for ulcer management and regular examination of feet by health professionals).

Other cost saving interventions include:

  • screening and treatment for retinopathy (which causes blindness)
  • blood lipid control (to regulate cholesterol levels)
  • screening for early signs of diabetes-related kidney disease and treatment.

Di·a·be·tes mel·li'·tus (DM),

DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L) 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. see also insulin resistance


Find a Specialist Find a Specialist

If you need medical advice, you can look for doctors or other healthcare professionals who have experience with this disease. You may find these specialists through advocacy organizations, clinical trials, or articles published in medical journals. You may also want to contact a university or tertiary medical center in your area, because these centers tend to see more complex cases and have the latest technology and treatments.

If you can’t find a specialist in your local area, try contacting national or international specialists. They may be able to refer you to someone they know through conferences or research efforts. Some specialists may be willing to consult with you or your local doctors over the phone or by email if you can't travel to them for care.

You can find more tips in our guide, How to Find a Disease Specialist. We also encourage you to explore the rest of this page to find resources that can help you find specialists.



Comments:

  1. Vudojas

    You are not right. I'm sure. I can defend my position.

  2. Chinua

    I know how to act, write in personal

  3. Giollabrighde

    Yes you are a storyteller

  4. Benedictson

    More of these blog posts.

  5. Farran

    the phrase is deleted



Write a message