Category Archives: Metabolic Diseases

Diabetes and Frozen Shoulder

Among the numerous complications frequently connected with diabetes, one of the foremost mystifying and painful is the frozen shoulder. Adhesive capsulitis, the condition’s biological term, is a pathological condition of the shoulder joint which causes the painful and gradual loss of motion.

The connective tissue of the shoulder joint inflames and stiffens, causing chronic pain, limiting mobility and disturbing sleep. The associated pain varies between sharp stings that radiate through the bicep to dull ache.

Link between diabetes and frozen shoulder:

There’s no conclusive connect link between the shoulder condition and the disease. Few studies indicate frozen shoulder is caused by glycosylation of the collagen in the shoulder joint.

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What Happens to the Shoulder?

Adhesive capsulitis is characterized by three stages, in spite of the fact that the severity and length of the stages may vary from individuals to individuals.

  • Stage One: Freezing – The most painful stage of the condition. During this stage, there’s a slow onset of pain coinciding with a progressive reduction in the range of motion (ROM) of the shoulder. Even simple movements like behind the back or reaching above the head are accompanied by tremendous pain and cramping.
  • Stage Two: Frozen- There’s a slow reduction of pain during this stage, but stiffness remains.
  • Stage Three: Thawing- During this final stage, there’s a gradual enhancement in ROM, as well as a lessening of stiffness and pain.

Treatment:

Frozen shoulder sees a wide extend of treatments. Diagnosis for the condition involves a physical exam, MRI, and x-ray, which is best for distinguishing soft tissue issues. Once diagnosed, physicians can advise an assortment of approaches, including physical therapy, surgical manipulation, steroid injections, and even supervised neglect.

Physical therapy is the foremost treatment for frozen shoulder. Therapists devise a particular exercise and stretching regimen to address the limited motion, restricted rotation, pain and strength. The regimen frequently utilizes heat and can take few weeks or even months for recognizable improvement.

Frozen shoulder proceeds to confuse health experts, and, surprisingly, there’s no way to prevent it. Early detection and proper treatment can allow a patient with diabetes to avoid the most painful and consequences of the condition.

 

Bioartificial pancreas – A recent advancement in the treatment of Diabetes

A bioartificial pancreas—a device that supports and encapsulates islets of Langerhans— replaces the beta cells and islets which were destroyed by type 1 diabetes. Implanted in the peritoneal cavity or under the skin, it contains approximately a million islets. It responds to changing blood glucose levels by releasing hormones, mainly insulin.

Every bioartificial pancreas is manufactured from non-living and living components. The living component is the islets, which secrete insulin concurring to typical physiology by sensing glucose levels. The non-living component shields the islets from the diabetic’s body and its destructive immune mechanisms, however grants the islets inside to thrive.

There are several types of bioartificial pancreas which includes microencapsulated, or coated islets are the first-generation bioartificial pancreas. Their advantage is that nutrients can effectively move into the islets and insulin can move out. Among the downsides is that they are difficult to remove because they don’t remain in one place.

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Macroencapsulation, another type, bunches islets cells together in a larger package. Such gadgets tend to be more stable and effectively extricated, but—at slightest in their earlier capsule form—may limit the free passage of insulin and nutrients. This starves the beta cells and hinders the objective of controlling blood glucose.

There are many technical challenges associated in using bioartificial pancreas. They are

  • Avoiding the immune response. The implemented bioartificial pancreas incites a fibrotic reaction, which restricts the islets from getting nutrition and thereby bioartificial pancreas passes on of starvation.
  • Enabling oxygen to enter to the core of the device. The measurements of most bioartificial pancreases don’t permit free passage of vital oxygen.
  • Fabricating the device without harming the islets. In some cases the process destroys numerous islets for the bioartificial pancreas to function.
  • Placing the device in close proximity to blood vessels, which provide nutrients and oxygen to the islets and carry secreted insulin to the rest of the body.

Different procedures are being investigated to extend the life and efficiency of transplanted islets. A few researchers are endeavouring to construct into the device helpful biochemical nutrients that release gradually. Other are centering on the shape and configuration of the bioartificial pancreas.

 

 

Obesity and Infertility

Obesity and Infertility

Excess weight is connected to many adverse health consequences including heart disease, diabetes, back and joint problems, and many other conditions. But now there is growing understanding that it moreover affects fertility.

Obesity affects the hormonal balance

When the Body Mass Index goes into the obese category (BMI of 30 and above), hormonal changes may happen in the body. Menstrual cycle is controlled by a fine hormonal balance. Obese and overweight women have higher levels of a hormone known as leptin, which is produced in fatty tissue. This can disrupt the hormone balance and lead to diminished fertility.

The amount and distribution of body fat influence the menstrual cycle through a run of hormonal mechanisms. The more abdominal fat and the more excess weight, the more prominent the risk of fertility difficulties.

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Obesity also leads to insulin resistance

The hormonal imbalance that comes with obesity frequently leads to insulin resistance. That is a major hazard factor for diabetes — but it also can create abnormal menstrual cycles and affects your fertility. Insulin resistance can lead to anovulation, in which female body does not produce eggs properly.

Obesity affects natural as well as assisted pregnancies

Obesity makes it more difficult to end up pregnant, even when utilizing natural ways or by artificial reproductive technologies such as in vitro fertilization (IVF). It also enhances your risk for a miscarriage. This issue may be caused by the hormonal issues noted above or because of body producing destitute quality eggs.

Obesity decreases the partner’s fertility, too

Although much of the obesity and infertility is on women, it absolutely influences men, too. For men, obesity leads to a drop in testosterone, which can lead to infertility. On top of that, erectile dysfunction happens at a higher rate among obese men. This can be likely due to a combination of factors. These include hormonal issues, sexual dysfunction and other well-being conditions linked to obesity such as sleep apnoea and type 2 diabetes.

Chances of success can be improved by losing weight. As you lose weight, the hormonal imbalances and other impacts of obesity begin to diminish. Start on a healthy path by incorporating positive way of life changes which includes regular exercise and more advantageous nourishment choices.

Diabetes Contributes to Cholesterol Metabolism

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Diabetes mellitus is the most frequent endogenous cause of fat metabolism-disorder. Cholesterol metabolism is abnormal in diabetes. Total plasma cholesterol is increased, and more subtle indices of sterol homeostasis are also disturbed.

Hypertriglyceridemia in diabetes is due to an increase of chylomicrons, triglyceride-carrying lipoproteins and the very-low-density lipoproteins. In type I-diabetics the pathogenesis for hypertriglyceridemia is about decreased activity of the lipoproteinlipase, reduced chylomicron-clearance and the impeded degradation of VLDL. More often in non-insulin-dependent diabetics LDL-cholesterol-levels can be seen lifted and HDL-cholesterol-concentration decreased in correlation with the metabolic control. Primary hyperlipoproteinemia shows up regularly in diabetics, but this can be clarified with the association with obesity in type II-diabetics.

Dyslipidaemia in T2D is characterised by several strictly linked anomalies: increased fasting and postprandial triglycerides (TG), a noteworthy decrease in high‐density lipoprotein (HDL) cholesterol and an increment in smaller low‐density lipoprotein (LDL) and HDL particles. The increase in plasma TG is to a great extent clarified by the increased production of TG‐rich; large‐sized VLDL in particular. The insulin resistant liver fails to inhibit lipid attachment to pre‐VLDL molecules and synthesises larger‐sized VLDL at a more prominent rate. Large TG‐rich; VLDL enhances the transfer of core lipids between VLDL, LDL, and HDL with increased formation of smaller LDL and HDL.

Also, the elevated postprandial TG that is frequently shown in patients with T2D may be connected to insulin resistance. Therefore, the abatement of hyperglycaemia and insulin resistance ought to be one of the most treatment destinations to address dyslipidaemia in patients with diabetes.

Also HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, is elevated in small intestine, and diminished in liver in diabetic rats. These changes in reductase activity are due to hyperphagia (increased caloric and/or cholesterol intake), not to insulin deficiency alone, since diabetic rats confined to a typical food intake have normal reductase activity in small intestine and liver. It shows that increased input of dietary and newly synthesized cholesterol by the small intestine raises plasma cholesterol level and quells reductase activity in liver of chronically diabetic rats.

On the whole, diet plays a central role in the diabetic’s cholesterol homeostasis. The hyperphagia of test diabetes increases net cholesterol intake and increased HMG-CoA reductase in a hypertrophic small intestine.

Diabetes Contributes to Cholesterol Metabolism

1

Diabetes mellitus is the most frequent endogenous cause of fat metabolism-disorder. Cholesterol metabolism is abnormal in diabetes. Total plasma cholesterol is increased, and more subtle indices of sterol homeostasis are also disturbed.

Hypertriglyceridemia in diabetes is due to an increase of chylomicrons, triglyceride-carrying lipoproteins and the very-low-density lipoproteins. In type I-diabetics the pathogenesis for hypertriglyceridemia is about decreased activity of the lipoproteinlipase, reduced chylomicron-clearance and the impeded degradation of VLDL. More often in non-insulin-dependent diabetics LDL-cholesterol-levels can be seen lifted and HDL-cholesterol-concentration decreased in correlation with the metabolic control. Primary hyperlipoproteinemia shows up regularly in diabetics, but this can be clarified with the association with obesity in type II-diabetics.

Dyslipidaemia in T2D is characterised by several strictly linked anomalies: increased fasting and postprandial triglycerides (TG), a noteworthy decrease in high‐density lipoprotein (HDL) cholesterol and an increment in smaller low‐density lipoprotein (LDL) and HDL particles. The increase in plasma TG is to a great extent clarified by the increased production of TG‐rich; large‐sized VLDL in particular. The insulin resistant liver fails to inhibit lipid attachment to pre‐VLDL molecules and synthesises larger‐sized VLDL at a more prominent rate. Large TG‐rich; VLDL enhances the transfer of core lipids between VLDL, LDL, and HDL with increased formation of smaller LDL and HDL.

Also, the elevated postprandial TG that is frequently shown in patients with T2D may be connected to insulin resistance. Therefore, the abatement of hyperglycaemia and insulin resistance ought to be one of the most treatment destinations to address dyslipidaemia in patients with diabetes.

Also HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, is elevated in small intestine, and diminished in liver in diabetic rats. These changes in reductase activity are due to hyperphagia (increased caloric and/or cholesterol intake), not to insulin deficiency alone, since diabetic rats confined to a typical food intake have normal reductase activity in small intestine and liver. It shows that increased input of dietary and newly synthesized cholesterol by the small intestine raises plasma cholesterol level and quells reductase activity in liver of chronically diabetic rats.

On the whole, diet plays a central role in the diabetic’s cholesterol homeostasis. The hyperphagia of test diabetes increases net cholesterol intake and increased HMG-CoA reductase in a hypertrophic small intestine.

Metabolic syndrome

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Metabolic syndrome could be a cluster of conditions such as insulin resistance, clustering of abdominal obesity, high blood sugar, high blood lipids and hypertension, and increased risk of clotting, stroke, predisposing individuals to diabetes and coronary heart diseases.

Symptoms of metabolic syndrome includes: visceral, central, abdominal obesity, particularly, a waist size of more than 35 inches in women and more than 40 inches in men, blood pressure of 130/85 mm/Hg or above, fasting blood glucose levels of 100 mg/dL or above, High-density lipoprotein (HDL) cholesterol levels of 40 mg/dL or less for men and 50 mg/dL or less for women, blood triglycerides levels of 150 mg/dL or higher.

High blood pressure, high blood glucose levels and cholesterol and lipid abnormalities can often be targeted early with lifestyle measures. Losing weight, especially within the upper body can be a successful treatment. A few measures for preventing and treating abnormal cholesterol and other perspectives of metabolic syndrome include: taking regular exercise, avoiding smoking, reducing alcohol intake and eating a “heart-healthy diet” that is low in fat, sugar and sodium.

The diet suggested for preventing and treating metabolic syndrome (mainly to prevent hypertension) is constraining intake of saturated fats and total fats, red meats, sodium and sweetened foods and drinks, consuming bounty of fruits and vegetables, fish, whole grains, and nuts.

Metabolic syndrome, sometimes truncated to MetS, can begin in childhood, alongside early obesity, high blood pressure, dyslipidemia and high blood pressure. Unavoidable risk factor, such as family history, can increase the chance of developing some components. In any case, lifestyle choices can impact all these factors.

Symptoms such as insulin resistance don’t essentially go with obesity or indicate metabolic syndrome. Insulin resistance is a feature of obesity and metabolic syndrome, and it can lead to type 2 diabetes and cardiovascular disease, but it can moreover be a sign of other conditions. Examples include polycystic ovary syndrome (PCOS), Cushing’s disease, chronic kidney disease and nonalcoholic fatty liver disease.

Other problems that are some of the time related with metabolic syndrome, insulin resistance, and high blood sugar include blood clotting defects and low-level inflammation. These can too contribute to the development of cardiovascular disease.

Structure of protein pair provides blueprint for future drugs

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Researchers visualize that SOCS1 protein can switch off cell signalling to decrease the immune responses and hence blocks the development of cancer.

The structure of SOCS1 binds to its partner protein JAK  at the atomic-level guiding the development of drugs which are capable of altering disease-causing cell signalling pathways and can also prove as the applications for treating some blood cancers, including leukaemia’s.

AT A GLANCE

  • SOCS1 protein can switch off cell signalling to reduce immune responses and hence blocking the growth of cancer.
  • Structural biology is used to visualise SOCS1 binding to JAK proteins.
  • The advancement of new drugs altering the JAK activity is given by the detailed structure which increases or decreases the cell responses along with applications in cancer treatments.

 SWITCHING OFF SIGNALLING

The structure of the protein pair revealed for the binding of SOCS1 to JAK proteins to disable signalling.

This explaines why JAK proteins cannot signal when bound to SOCS1. This information helps in development of innovative medicine targeting the cell signalling pathway.

A BLUEPRINT FOR NEW MEDICINES

SOCS1 and JAK proteins are implicated in driving diseases including cancer and inflammatory conditions.

The cancer-like conditions called Myelo Proliferative Neoplasms (MPNs) is linked with JAK signalling, including polycythemia vera, essential thrombocythemia and primary myelofibrosis and certain acute childhood leukaemias.

Medicines are used for treating MPNs that inhibits the JAK signalling, but they can only manage the disease and cannot cure it. New medicines for these conditions are needed and it is foreseen that a drug designed to mimic the SOCS1 protein to switch off JAK proteins will be more effective treatment.

SOCS1 binding to JAK proteins normally applies a restriction to immune responses which is good thing for a healthy person.

Under certain conditions, releasing this restriction could be a key to enhance immune responses. This approach to boost the immune response could be the key in improving immunotherapies for treating cancer. Designing a drug that inhibits SOCS1 may boost anti-cancer immune responses which potentially improving anti-cancer immunotherapies.

Abnormal lipid metabolism in fat cells predicts future weight gain and diabetes in women

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The inefficient breakdown of fats foretells later metabolic complications such as type 2 diabetes in women and weight gain. Low levels of hormone-stimulated lipolysis — a biochemical process by which triglycerides (Cholesterol, lipid) are broken down into energy-rich fatty acids — were related with weight gain and metabolic problems in future. To detect impedances in hormone-stimulated lipolysis, researchers created an algorithm using clinical and blood measures.

Researchers believed that their proposed algorithm could be helpful in identifying subjects with a high risk of becoming overweight or obese. These findings may well be utilized by clinicians to determine who would benefit the most from intensified lifestyle interventions such as physical activity, which improves hormone-stimulated lipolysis and may therefore prevent metabolic disturbances and fat accumulation.

Researchers took biopsies of subcutaneous fat tissue from healthy and non-obese 89 women, and followed up 13 years later. The women who gained weight within the between times showed a 50% diminish in hormone-stimulated lipolysis and a 50% increment in spontaneous lipolysis compared with weight-stable individuals. Moreover, lower expression of genes involved in regulating lipolysis was related with later weight gain.

Therefore it can be concluded that insufficient lipolysis which cannot be satisfactorily quickened by hormone stimulation, may shift the balance in lipid turnover towards uptake, which facilitates fat mass accumulation.

Instead of tissue biopsies, the researchers next constructed an algorithm to estimate hormone-stimulated lipolysis based on clinical and blood measures. To distinguish parameters for this metabolic measure, researchers analysed information from 1,045 subjects. They found six parameters which included fasting plasma HDL cholesterol, waist circumference, fasting plasma adrenaline, fasting serum insulin, body weight and fasting plasma glycerol divided by total body fat.

In a subset of 226 subjects, the algorithm predicted high or low lipolytic activity with approximately 75% specificity and greater than 80% sensitivity. When tested in a separate group of 14 individuals, the algorithm corresponded well with measured levels of hormone-stimulated lipolysis and predicted weight changes over time.

These results suggest that the algorithm could be used to estimate hormone-stimulated lipolysis rather than tissue biopsies in a routine clinical practice. However, future studies are needed to implement the algorithm in larger groups of people and to decide whether the findings of this study also apply to men.

Drinking Camomile Tea Could Help Control or Prevent Diabetes

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Camomile (yellow flower) is made into a tea, enjoyed before bed – is an exceptionally interesting plant. That bedtime herbal tea may be doing numerous individuals a part of great. It was as of late found that this flower may control or prevent diabetes. Camomile is utilized to give a shiny yellow colour on wool, cotton and other natural textiles.

Nature makes a cocktail of different compounds in the dye plants. The chemistry and proportion of these particles can give critical data approximately which plant species was utilized to colour the strands. Apart from dye industry it is also used as a food, most people will be familiar with camomile’s use as an herbal tea, often associated with supporting sleep. Undoubtedly acknowledgment of its therapeutic properties as a relaxant and sedative is exemplified by its listing as an official drug in the pharmacopoeias of 26 countries, including the UK. But numerous didn’t figure it out that it possibly has other dietary benefits. German chamomile has been taken for stomach related issues since at slightest the primary century.

 The interface between dietary components and carbohydrate absorption was considered by the analysts and they found how certain common compounds can offer assistance to control blood glucose levels. They had screened several plant extracts and identified German chamomile (Matricaria chamomilla) as exceptionally successful in controlling diabetes in 2017. But they couldn’t get it which compound in specific was responsible for this activity. All pondered how the research on natural dyes in camomile could help with this.

 Researchers applied the techniques that they had developed for extraction of historical textiles and analysis of camomile flowers. Working together, they discovered four particular compounds that are active in camomile and able to control carbohydrate digestion. Out of four two of the compounds are yellow colorants and the other two compounds had been already recognized by other analysts. Studies went on to find the contribution of these four compounds to the overall bioactivity of camomile, and found that, taken together, they were able to balance carbohydrate digestion and absorption. So on the whole, drinking camomile tea may be helpful in controlling or even preventing diabetes.

International Conference on Diabetes and Cholesterol Metabolism

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Metabolic Diseases 2018 enlightens the recent advancements related to Diabetes, Cholesterol Metabolism and Metabolic Diseases and aims on sharing the knowledge of the expertise in this field where the new generation scholars and researchers can increase their knowledge related to diabetes and metabolic diseases. This conference welcomes all the Eminent Diabetologists, Researchers, Endocrinologists, Doctors, Physicians, Scientists, Diabetes Societies and Associations, Dieticians, Epidemiologists, Business Professionals, Academic Professionals, Students, Medical & Pharmacy Companies. It is an opportune time to renew contacts and discuss problems of mutual interest with delegates from different regions of the countries.

The “International Conference on Diabetes and Cholesterol Metabolism” is going to be held on October 15-17, 2018 at Dubai, UAE. The upcoming conference will be organized around the theme Be Stronger than Diabetes. The purpose of 3 days conference is to bring together researchers from around the world who are interested in exploring the links between diabetes, cholesterol metabolism and metabolic diseases. The conference will focus on topics such as diabetes mellitus, gestational diabetes, diabetes complications, endocrinology, obesity, metabolic syndrome, epidemiology of diabetes, diabetic education, cholesterol and diabetes, cholesterol metabolism, lipid metabolism, cardiovascular diseases, hypercholesterolemia, hyperlipidemia, and recent advances in treatments &therapies.

Diabetes is prevalent in all parts of the world. Number of people suffering from Diabetes disorders continues to rise each year. As reported by the World Health Organization (WHO), on an average 1 out of every 13 people are diagnosed globally with Diabetes each year and also projects that diabetes will be the 7th leading cause of death in 2030. Around 60% of the populations effected with Diabetes diseases are uncaring of the situation. The importance of both diabetes and their comorbidities will continue to increase as the population ages.

Metabolic Diseases 2018 will feature the latest developments in research, diagnosis, prevention and management of metabolic diseases, diabetes, new insulin analogues and new technologies, devices for diabetic prevention, for treating obesity and many more. Not only will this innovative conference enhance your practical and theoretical knowledge, it will provide you with the unique opportunity to network with a wide range of professionals in the field of diabetes technologies and treatments.