Type 2 diabetes etiology and pathogenesis,diabetes type 2 pathophysiology flow chart,diabetes care treatment guidelines who,global guidelines for type 2 diabetes 2012 32bit - New On 2016

A 10- year-old child has been diagnosed with Juvenile diabetes mellitus (type 1 diabetes mellitus). This is a disorder of carbohydrate metabolism caused by insulin deficiency. Many common diseases are caused by a combination of environmental factors and genetic factors, and are described as multifactorial diseases. Approximately one-third of the disease susceptibility of type 1 diabetes mellitus is due to genes and two-thirds due to environmental factors.
The global incidence of type 1 diabetes is increasing (approximately 3% each year).This form of diabetes is immune-mediated in over 90% of cases and idiopathic in less than 10%. The autoimmune destruction of pancreatic ?-cells leads to a deficiency of insulin secretion. Children of diabetic parents are at increased lifetime risk for developing type 1 diabetes. Sex linked disorders predominantly occur in males or females, in contrast to the equal distribution in males and females in type 1 diabetes mellitus. Congenital disorders are present at the time of birth, in contrast to type 1 diabetes mellitus which usually presents during childhood. Sporadic disorders have no genetic predisposition and do not cluster in families except by chance or through similar environmental exposure. Mendelian disorders are completely determined by the genotype of an individual, and exhibit 100 % concordance in identical twins.
Please help Biochemistry for Medics by "CLICKING ON THE ADVERTISEMENTS" every time you visit us. Type 2 DM • Inception of disease begins with development of key metabolic abnormality, insulin resistance. Insulin • A polypeptide hormone secreted by the islet of Langerhans in ?-cells of the pancreas.
Insulin’s function • Standard metaphor (Lock & Key) Insulin (the key) must be bound to target cell (the lock) in order for glucose to enter the target cell from the bloodstream. Insulin Resistance • Metabolic abnormality that triggers the onset of type 2 DMNormal amount of insulin becomes inadequate for proper absorption of blood glucoseThe body’s energy absorption system becomes inept • Hypothesized triggers of IR 1 in 10 people have genetic code for IR. Treatment of type 2 DM • First goal is to eliminate symptoms and stabilize blood glucose levels. Meglitinides • Also stimulates insulin • Repaglinide secretion by ? cells • Similar mechanism of action to Sulfonylureas.
Thiazolidinediones • Improves insulin sensitivity (adipose tissue)• Bind to steroid hormone nuclear receptor family- peroxisome proliferator activated receptors [PPARs]- specifically PPAR? isoform. Future of type 2 DM • Complications can be prevented through proper diet and exercise • Goal of future drug research is normalizing blood glucose and decreasing insulin resistance • Proper education is necessary.
But a study published in the journal Diabetologia, reveals how having type 2 diabetes can cause health to spiral downwards quickly – taking a person from good health to the grave in a year.
Researchers from University of Copenhagen and Steno Diabetes Center identified that cancer patients who also suffer from diabetes have less chances of survival compared to cancer patients without diabetes.
The main aim of this research was to identify differences in survival among cancer patients with diabetes prior to cancer diagnosis compared to cancer patients without diabetes.
The best way to study this was the association between medications that lower glucose levels in the blood and its effect on survival.
Patients with diabetes for 2 years and taking insulin at the time of cancer diagnosis have nearly 4 times higher mortality rate a year after cancer diagnosis! Other patients who took oral medications or did not take any medications for diabetes showed a 10 percent higher risk of mortality a year after cancer diagnosis. All this proves one thing – evidence points out that survival after cancer in diabetics is significantly higher compared to people without diabetes.
This is just one more reason why you need to address type 2 diabetes quickly and aggressively using natural, methods. A simple change in diet was all that my mother needed to reverse her Type 2 Diabetes within a month.
But first, I’d really appreciate it if you click the Facebook button below and share this articles with your friends. Acanthosis Nigricans is a skin disorder that makes the folds of the skin thicker, darker and velvety.
Though the disorder can strike a person of any gender, descent and age, it is more common in people of African origin. The symptoms of Acanthosis Nigricans mainly consist of the skin turning darker and more velvety. Lymphoma or cancerous conditions of the genitourinary or gastrointestinal tracts can also result in Acanthosis Nigricans. Use of medicines like contraceptive pills and human growth hormones can also lead to this disease.
Acanthosis Nigricans can be diagnosed by an expert medical professional by mere physical observation.
Acanthosis Nigricans generally disappears after a few days without the need of any treatment.
If obesity is found to be a cause, the affected person may have to take up daily exercise to lose weight fast.
When Acanthosis Nigricans affects people older than 40 years, it usually results from an internal malignancy or Adenocarcinoma of the uterus or Gastrointestinal tract.
Mild cases of can be treated using a Glucocorticoid Acanthosis Nigricans cream like Panolog. If you are having Acanthosis Nigricans cases in your family or suffering from the disease yourself, it is best to wait for a week or two.

When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases, this is known as ketonemia. The disease is often preceded by viral infection with inflammation of the beta cells of pancreas, but also exhibits genetic predisposition with a 40-50% concordance rate in monozygotic twins and clustering in families.
There have been a number of different hypotheses including infections with certain viruses (rubella, Coxsackie B4) and consumption of cow’s milk. It is this loss of insulin secretion (figure) that leads to the metabolic derangements associated with IDDM (insulin dependent diabetes mellitus) Less than 10% of subjects have no evidence of pancreatic B cell autoimmunity to explain their insulinopenia and ketoacidosis.
A child whose mother has type 1 diabetes has a 3% risk of developing the disease and a 6% risk if the child’s father has it. If you interesting in "Type 2 Diabetes Mellitus" powerpoint themes, you can download to use this powerpoint template for your own presentation template. Acetohexamide • Binds and closes K+ Chlorpropamide channels on ? cells causing influx of Ca2+ Tolbutamide which triggers the release Tolazamide of insulin. Attaches to K+ channel at a different binding site • Insulin efflux is glucose • Nateglinide dependent. Another area of study was to identify how this association changes with duration of diabetes and time since cancer diagnosis. The patients were then divided into four groups: those who didn’t have diabetes, those who had diabetes but didn’t take any medications, those who took oral hypoglycemic agents (blood sugar-lowering medications) and those who took insulin. Prevention and treatment of type 2 diabetes: Current role of lifestyle, natural product, and pharmacological interventions. Differential adaptation of human gut microbiota to bariatric surgery-induced weight loss: Links with metabolic and low-grade inflammation markers.
Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal. Modulation of glucagon-like peptide 1 and energy metabolism by inulin and oligofructose: Experimental data. Inulin-type fructans modulate gastrointestinal peptides involved in appetite regulation (glucagon-like peptide-1 and ghrelin) in rats.
Involvement of endogenous glucagon-like peptide-1(7-36) amide on glycaemia-lowering effect of oligofructose in streptozotocin-treated rats. Oligofructose promotes satiety in rats fed a high-fat diet: Involvement of glucagon-like Peptide-1. Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon-like peptide-1 receptor.
Folic acid supplementation during the juvenile-pubertal period in rats modifies the phenotype and epigenotype induced by prenatal nutrition.
Developmental changes of gut microflora and enzyme activity in rat pups exposed to fat-rich diet. Diet-induced obesity is linked to marked but reversible alterations in the mouse distal gut microbiome. High-Fat diet determines the composition of the Murine gut microbiome Independently of obesity. Shifts in clostridia, bacteroides and immunoglobulin-coating fecal bacteria associated with weight loss in obese adolescents.
Distinct composition of gut microbiota during pregnancy in overweight and normal-weight women. Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial. The probiotic Lactobacillus gasseri SBT2055 inhibits enlargement of visceral adipocytes and upregulation of serum soluble adhesion molecule (sICAM-1) in rats. Effects of Lactobacillus gasseri BNR17 on body weight and adipose tissue mass in diet-induced overweight rats.
Antiobesity effects of Bifidobacterium breve strain B-3 supplementation in a mouse model with high-fat diet-induced obesity. Evidence that the trans-10, cis-12 isomer of conjugated linoleic acid induces body composition changes in mice. Human originated bacteria, Lactobacillus rhamnosus PL60, produce conjugated linoleic acid and show anti-obesity effects in diet-induced obese mice. Antiobestity effect of trans-10, cis-12-conjugated linoleic acid-producing Lactobacillus plantarum PL62 on diet-induced obese mice.
Recombinant lactobacilli expressing linoleic acid isomerase can modulate the fatty acid composition of host adipose tissue in mice.
High polyphenol, low probiotic diet for weight loss because of intestinal microbiota interaction. The effect of probiotic Dahi Containing Lactobacillus acidophilus and Lactobacillus casei on gastropathic consequences in diabetic rats.
Probiotic modulation of symbiotic gut microbial-host metabolic interactions in a humanized microbiome mouse model.
Decreased fat storage by Lactobacillus paracasei is associatedwith increased levels of angiopoietin-like 4 protein (ANGPTL4). Colonic fermentation influences lower esophageal sphincter function in gastroesophageal reflux disease. Density distribution of free fatty acid receptor 2 (FFA2)- expressing and GLP-1-producing enteroendocrine L cells in human and rat lower intestine, and increased cell numbers after ingestion of fructo-oligosaccharide. Dietary non-digestible carbohydrates promote L-cell differentiation in the proximal colon of rats.

Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Dietary modulation of clostridial cluster XIVa gut bacteria (Roseburia spp.) by chitin-glucan fiber improves host metabolic alterations induced by high-fat diet in mice. Comparison of different fibers for in vitro production of short chain fatty acids by intestinal microflora. Dietary fiber modulates intestinal proglucagon messenger ribonucleic acid and postprandial secretion of glucagon- like peptide-1 and insulin in rats. Weight loss during oligofructose supplementation is associated with decreased ghrelin and increased peptide YY in overweight and obese adults. Acute effects of intravenous and rectal acetate on glucagon-like peptide-1, peptide YY, ghrelin, adiponectin and tumour necrosis factor-alpha.
Adaptation of colonic fermentation and glucagon-like peptide-1 secretion with increased wheat fibre intake for 1 year in hyperinsulinaemic human subjects. Changes in gut microbiota control inflammation in obesemice through amechanism involving GLP-2-driven improvement of gut permeability. Inulin-type fructans with prebiotic properties counteract GPR43 overexpression and PPARgamma-related adipogenesis in the white adipose tissue of high-fat diet-fed mice.
The fermentable fibre inulin increases postprandial serum short-chain fatty acids and reduces free-fatty acids and ghrelin in healthy subjects.
Effects of a soluble dietary fiber supplementation with NUTRIOSE® on risk factors of the metabolic syndrome in Chinese male adults.
M.,Sunita Grover,Virender Kumar Batish Critical Reviews in Food Science and Nutrition. Lyon,Veronica Kacinik Current Obesity Reports. In rare cases, other areas of the body such as palms, lips and soles of the feet may also be affected.
Excess insulin results in production of melanocytes, cells that are the cause of pigmentation in humans. Many obese people suffer from diabetes and endocrine disorders which can trigger Acanthosis Nigricans. However, skin biopsies, X-Rays and endoscopy may be recommended if the doctor suspects diabetes or any cancerous condition to be the cause.
However, persistent symptoms of the disease call for an effective Acanthosis Nigricans cure. For obese people with diabetes Acanthosis Nigricans recovery can be faster with rapid loss of weight.
Obese people are frequently seen to suffer from Insulin Resistance, which arises due to Type 2 Diabetes or Pre-Diabetes. Adenocarcinoma can also affect other regions of the body such as breast, prostate gland, stomach, ovary or lung.
This is basically a corticosteroid cream which has antibacterial, antifungal and anti-inflammatory properties. The risk in siblings is related to the number of HLA haplotypes that the sibling shares with the diabetic parent. For viewing only, you can play with our flash based presentation viewer instead of downloading the ppt file.
When energy requirements are met, insulin in the bloodstream triggers the liver to absorb glucose and convert it into energy saving form glycogen. Glucagon-like peptide-1, and neurotensin responses to luminal factors in the isolated vascularly perfused rat ileum. A high insulin level can result from a number of disorders like pre-diabetes, diabetes and insulin resistance.
Check out these Acanthosis Nigricans images and see whether the patches on your skin are similar to the ones shown here.
In such situations, Acanthosis Nigricans can be a sign of life-threatening conditions in the body. Acanthosis Nigricans of the tongue or mucous membrane of the mouth is usually a sign of a tumor in the Gastrointestinal Tract. The disease mainly arises in canines due to Hypothyroidism, Hormonal imbalance, Food allergies and obesity. If one haplotype is shared, the risk is 6% and if two haplotypes are shared, the risk increases to 12–25%. Read on to know all about Acanthosis Nigricans, its causes, symptoms, diagnosis and treatment. Obese kids are also at a higher risk of developing Type 2 diabetes some years later in their lives.
Dietary modifications can help both Acanthosis Nigricans children and adults recover within a month. This percentage of genetically identical monozygotic twins who share this trait of diabetes mellitus provides a measure of the genetic contribution to the etiology. Vernon-Carter LWT - Food Science and Technology.

M logo quiz
Medical errors test answers 1-50
Natural cure for diabetes philippines convention
Gc 051ss chladni?ka lg


  1. Fellin

    Eats and don't put in a tone of time doing don’t have a food background or dietary background, they.


  2. Shadowstep

    Develop joint points in later saturated fatty acid content material of the take a look carb.