Type 2 diabetes a level biology youtube,when should a type 2 diabetic take insulin,indian vegetables for diabetic patients - Test Out


Type 2 Diabetes Mellitus is a chronic and systemic metabolic disorder distinguished by high blood glucose (hyperglycemia), insulin resistance, and insulin deficiency. The individual with Type 2 Diabetes typically goes undiagnosed for years because the onset is gradual and signs of hyperglycemia is not noticed.
The long-term presence of type 2 diabetes impacts the large and small blood vessels and nerves throughout the body. The insulin signaling pathway refers to the complex biological process of insulin reacting with target cells such as muscle, fat, or liver cells and the resulting intracellular effects that result, leading to various functional effects observed at the multicellular level. Insulin works by binding its specific receptor on cell surfaces throughout the body, such as on liver, muscle or adipose cells.[5] The insulin receptor is a tyrosine kinase protein that undergoes autophosphorylation of its tyrosine residues that located on its cytoplasmic face once activated by insulin. In total, the activation of the PI3K subpathway mediates several insulin-induced responses including GLUT4 activation, glycogen synthesis by inhibiting CSK-3 phosphorylation, and lipogenesis by up-regulation of fatty-acid synthase gene expression. MAPK is other main subpathway that is activated after IRS-1 and 2 phosphorylation that begins with small adaptor proteins Grb2 and SHP2 that lead to further substrate activation downstream. Insulin-mediated Glucose transport is primarily accounted for through the translocation of glucose transporters to the plasma membrane, most of which is GLUT4 within muscle and adipose cells. Most of glucose that enters human muscle in response to insulin is desposited as Glycogen (see Carbohydrate Storage: Glycogen for more information). The biochemical process of glycolysis reverses many of the steps of Glycogenesis with different enzymes[64]. The Immune System of the human body is comprised of two different systems, the aquired immune system and innate immune system.
The innate immune system is the body’s first-line of defense against invaders including infections and physical or chemical injury. Research has shown that circulating concentrations of acute-phase reactants is increased in type 2 diabetic patients when compared to nondiabetic subjects. The Insulin Resistance Atherosclerosis Study (IRAS)[37] investigated the relationships insulin resistance, cardiovascular risk factors, and cardiovascular disease in a multiethnic population across varying statuses of glucose tolerance. Research indicates that increased ROS levels are associated with altered mitochondrial morphology in both myotubes cultured in high glucose conditions and in diet-induced diabetic mice.[16] In addition, increased oxidative stress in mitochondria may contribute to increased lipid peroxidation and damage to cell membranes and DNA. Apoptosis is a genetically directed process of cell self-destruction marked by the fragmentation of nuclear DNA.[45] It is a form of cell death during which a programmed sequence of events leads to the elimination of cells without releasing harmful substances into the surrounding area. Evidence suggests that the release of cytochrome c from the mitochondria results from direct action of ROS on cardiolipin, a mitochondrial phospholipid which is located in the inner mitochondrial membrane.[17][52][53] During the early phase of apoptosis, mitochondrial ROS production is stimulated and cardiolipin is oxidized (loses electrons).
Although HbA1c is directly related to blood glucose levels, it is important to realize that blood glucose and HbA1c are not the same. A portion of the metabolic stress seen in Type 2 Diabetes may originate from myocellular fat storage.
A four month study investigating the relationship between insulin sensitivity (IS) and IMCL content in Zucker diabetic fatty rats (ZDF) confirmed the relationship between IS and IMCL content seen in humans. AMPK is a protein kinase, that combines signals to monitor and balance both systemic and cellular energy. At times of high energy demand the ? subunit rapidly responds to changes in the AMP to ATP ratio to maintain energy balance. AMPK is activated by physical activity in such a way that increased intensity results in increased activation. Reduction of AMPK activity promotes the development of insulin resistance and glucose intolerance, disturbs muscle energy balance during exercise, and decreases mitochondrial biogenesis (mitochondria’s ability to make ATP).[33] In insulin-resistant rodents, increased AMPK activity has been linked with improved blood glucose homeostasis, lipid profile and blood pressure. The microRNA miR-34a is highly expressed in patients with non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH) and type 2 diabetes. Diabetes is a disease that has reached epidemic proportions both internationally and within New Zealand.
To understand Diabetes we first need to recap how glucose (blood sugar) is normally regulated in our bodies. When blood glucose levels are low, insulin secretion is decreased, and the hormone glucagon is released from the pancreas instead. Depending on the type of Diabetes diagnosed, a mixture of diet, exercise and medication will be prescribed for the individual. If a Diabetic cana€™t keep their glucose levels in a safe range, they could develop a number of long term health complications.
This can cause damage to the smaller blood vessels in your body a€“ for example in your eyes (leading to blindness), toes (leading to amputations) and kidneys (leading to kidney failure).
To sum it up, Diabetes is bad news, and due to our over-indulgent and inactive lifestyle, it is more and more common these days.
Another possible connection has to do with an  important group of molecules in our body called Toll-like receptors, or  TLRs.
TLR-4 deficient mice, on the other hand, seem to be protected from insulin resistance, just like TLR-2 deficient mice.
But Andrea Caricilli and colleagues have decided to look at TLR-2 knockout mice in non-sterile conditions.
They then transplanted the microbiota from TLR-2 mutants which had insulin resistance to regular mice. There is a lot more to this paper than these two experiments: they have also investigated many other parameters, trying to come up with the chain of events that bacteria trigger when causing metabolic disease.
I was wondering how the high levels of antibiotics in animal feed would effect the gut bacteria in humans. Byte Size Biology is licensed under a Creative Commons Attribution-Share Alike 3.0 Unported License. Recent CommentsPolemica PLOS expoe intolerancia ao acesso aberto - SIBiUSP - Sistema Integrado de Bibliotecas da Universidade de Sao Paulo. Due to staffing limitations we are not able to offer telephone or email advice to parents of children. Each kidney contains around a million units called nephrons, each of which is a microscopic filter for blood.


Pyelonephritis (infection of kidney pelvis): Bacteria may infect the kidney, usually causing back pain and fever.
Glomerulonephritis: An overactive immune system may attack the kidney, causing inflammation and some damage. Kidney stones (nephrolithiasis): Minerals in urine form crystals (stones), which may grow large enough to block urine flow. Nephrotic syndrome: Damage to the kidneys causes them to spill large amounts of protein into the urine. Polycystic kidney disease: A genetic condition resulting in large cysts in both kidneys that impair their function. End stage renal disease (ESRD): Complete loss of kidney function, usually due to progressive chronic kidney disease.
Papillary necrosis: Severe damage to the kidneys can cause chunks of kidney tissue to break off internally and clog the kidneys. Diabetic nephropathy: High blood sugar from diabetes progressively damages the kidneys, eventually causing chronic kidney disease.
Interstitial nephritis: Inflammation of the connective tissue inside the kidney, often causing acute renal failure.
Minimal change disease: A form of nephrotic syndrome in which kidney cells look almost normal under the microscope. Nephrogenic diabetes insipidus: The kidneys lose the ability to concentrate the urine, usually due to a drug reaction. Individuals commonly experience visual blurring, neuropathic complications, infections, fatigue and significant blood lipid abnormalities.[2][12] Type 2 Diabetes is typically diagnosed when the patient is receiving medical care for another problem. Chronic hyperglycemia can lead to macrovascular disease, which affects the arteries supplying the heart, brain, and lower extremities.[2] Type 2 diabetes is also associated with the development of microvascular pathologies in the retina, renal glomerulus, and peripheral nerves.
Through PKB’s isoforms ?, ?, and ?, it plays role in mediating glycogen synthase kinase-3, metabolic actions of insulin, and Glut4 translocation.[8][66] It is debated whether PKB plays a significant role in insulin resistance with diabetes.
Mounting evidence has shown that PI3k and PKB activation participate in the stimulation of p70 S6k. Insulin increases the transporters’ cycle to and from the cell surface by promoting exocytosis and inhibiting endocytosis. Insulin causes stable Glycogen Synthase (GS) activation by causing dephosphorylation at multiple sites within the enzyme. Through these three subpathways, the insulin signaling pathway promotes GS and glycogen synthesis.
The aquired immune system is your immunity your body build up from being exposed to foreign invaders, and the innate immune system is the body's natural unspecific defense against new foreign invaders that the body has not built up immunity against. Participants demonstrated normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or type 2 diabetes mellitus.[37] Measures of insulin sensitivity and insulin secretion were obtained from all participants during two 4-hour visits, occurring approximately one week apart. Increased levels of ROS are a likely cause in a variety of pathophysiological conditions, including type 2 diabetes.[16] Oxidative stress to the mitochondria can come from many sources. The amount of hemoglobin that forms HbA1c depends on the amount of glucose that hemoglobin is exposed to over time.[22],[23] For example, hemoglobin exposed to high levels of glucose for long periods of time results in greater amounts of glycation. The Diabetes Control Card is a quick reference for patients diagnosed with diabetes to assess glucose control.
In muscle tissue, lipids are stored as either extramyocellular lipids (EMCL) or intramyocellular lipids (IMCL). An obese Zucker diabetic fatty rat has significantly higher IMCL concentrations than its lean counterpart. AMPK phosphorylates TBC1D1 which increases activity of GLUT4, resulting in increased glucose uptake. At the molecular level, miR-34a has been shown to exert its function through its effect on sirtuin 1 (SIRT1).
It is the leading cause of blindness, kidney failure and lower limb amputations in the world.A  So what is this horrible disease?
Insulin helps move glucose from the blood stream into our muscles and liver, and stores any extra glucose as fat.
On the flip side, when glucose levels get too high, the symptoms of Diabetes begin to appear. Diabetes cannot be a€?cureda€™, so the aim is to manage the disease by bringing glucose levels down into the normal range, and keeping them there!
Thick blood can also damage the blood vessels supplying your nervous system, causing loss of sensation and numbness, especially in your extremities like your feet.A  Maintaining healthy glucose levels over the long term will prevent or delay the onset of Diabetes complications. The following articles in this series will examine the two main types of Diabetes a€“ Type 1 and Type 2 in more detail, and discuss both the challenges and the benefits of training people with Diabetes. We really have to revise our definition of what a human (or any other animal or plant) is: we are not just a creatures of 10,000,000,000,000 cells containing the DNA we got from mother and father. Well, for one thing, we know that in obese people the bacterial population in the gut is different, and the different population of bacteria may lead to a vicious cycle contributing to obesity.
TLRs are a family of  membrane proteins that sense a wide variety of bacterial populations and activate our innate immune system. So a connection between these front-line sensors of the immune system and whole body metabolism is well-known. The thing about mutant TLR deficient mice, is that they are normally grown in sterile conditions because possible infections and because the uncontrollable gut microbes add uncontrolled variables to any experiment. Yes, there are mutant mice, but still: insulin resistance was turned off  by changing the types of microbes in the gut.
And what do you know: the regular mice then showed symptoms of insulin resistance and metabolic disease. It's possible to lose as much as 90% of kidney function without experiencing any symptoms or problems. A spread of bacteria from an untreated bladder infection is the most common cause of pyelonephritis.


Dehydration, a blockage in the urinary tract, or kidney damage can cause acute renal failure, which may be reversible. Although it's rarely dangerous, diabetes insipidus causes constant thirst and frequent urination. Raf phosphorylates MEK, a dual-specificity kinase of tyrosine and threonine that activates mitogen-activated protein kinase (MAPK). It has been shown that tyrosine kinase activity and IRS-1-protein phosphorylation are two essential processes in normal glucose transport. PKB has also been shown to directly inhibit GSK-3, a well-known inhibitor of GS, thereby promoting GS.
Ezymes responsible for Glycogenolysis 1 through 3 respectively: Glycogen phosphorylase, Phosphoglutomutase, Phosphoglutomutase, and Glucose-6 Phosphotase.
ROS are produced in larger amounts by islet cells from patients with type 2 diabetes than by those from non-diabetic patients.[17] Although some ROS are produced in the peroxisomes, the major source of ROS production in cells is the mitochondria.
This is directly related to continuous breakdown and replacement of erythrocytes in the body. EMCL is metabolically static, but IMCL stores are built up, mobilized, and used within hours. Glucose cannot enter your bodya€™s cells from the bloodstream by itself, so insulin acts like a a€?keya€™.
We have 10 times that many cells which are microbial, and we are only now beginning to understand how profoundly they affect us.
TLRs are like a first-defense warning station: they sense the bacterial enemy first, and, if needed, activate the proper defense mechanisms. I have posted before about how TLR-5 may control the type of gut bacteria mice have and, in turn, control their propensity for obesity.
What Caricilli and her colleagues discovered was quite the opposite of what was known so far: TLR-2 knockout mice were not protected from insulin resistance. The kidneys remove wastes, control the body's fluid balance, and regulate the balance of electrolytes. The MAPK pathway is well known within the insulin signaling cascade, but is not very sensitive to insulin or involved in most of the hormone’s important metabolic responses.[8] The MAPK subpathway has some evidence showing it functions to exert feedback regulation on the PI3k subpathway and is involved in the process of insulin resistance.
The PI3k subpathway functions to mediate glut4 activation, glycogen synthesis, and lipogenesis. Within these pathways, PI3k, PKB, and the atypical PKCs play an particularly key roles in the process of glucose uptake into cells. MAPK has been implicated in activating GS through phosphorylation of p90 Ribosomal S6 kinase 2 (p90 rsk2) and glycogen bound protein phosphatase-1 (PP1G) downstream.
The later branch is implicated GS promotion by inhibition of the well-established inhibitor of GS, GSK-3.
During times of high glucose uptake, increased amounts of glucose-6-phosphate (G6P) leads to an increase in glycogen synthesis. Once released into the blood, insulin binds to insulin receptors (the a€?keyholesa€™) located on the cell walls, a€?unlockinga€™ the cell and allowing the glucose to enter.
Researchers studying TLR-2 have created knockout mice lacking TLR-2, and they discovered is that many of TLR-2 knockout mice do not develop insulin resistance when fed with a high-fat diet. Or, maintain full control of the experiment and sacrifice a simulation whatever they are trying to model.
But the bottom line again supports what has been shown in other studies: the bacteria that live in our gut are responsible for our metabolism, and it is the interaction between the bacteria and our immune system that not only protects us from pathogens, but also protects us (or not) from metabolic disease.
For example, comparing mostly beef & pork consumers (where antibiotics in the feed are legal, at least in the US), and poultry consumers (which are mostly antibiotic free). As the kidneys filter blood, they create urine, which collects in the kidneys' pelvis -- funnel-shaped structures that drain down tubes called ureters to the bladder. In contrast, the downstream constituents of PKB such as p70 S6k have been shown to have no immediate effects on glucose uptake. PP1G has many phosphorylation sites that insulin has been shown to augment, but its exact role in GS promotion is not fully understood. How much do we really need to understand about the disease to train our Diabetic clients effectively?
This glucose can either be used immediately as energy or stored as glycogen or fat for future use. Think about it: all the McCrap you can eat, yet your blood sugar level remains normal (although you still grow fat). However, it would be very hard to separate other factors, such as overall calorie intake (higher in beef & pork than in poultry), associated lifestyle, etc.
The MAPK subpathway may serve to regulate the PI3k subpathway and may be involved in insulin resistance, but more research is needed to prove this. Indirect activators (metformin, dinitrophenol (DNP), and rotenone) work by increasing AMP:ATP ratio, compound C works by inhibiting activation of AICAR. SIRT1 feedback inhibits miR-34a in several ways: it deacetylates p53 and inhibits p53-dependent transcriptional activation of mir-34a. That is because a model (in our case, mutant TLR mice), is somewhat removed from the real thing anyway: mutant TLR-deficient are basically a  an artificial construct used to investigate the effect of knocking out a TLR from the mouse, so hopefully we can draw conclusions about humans. To check that, the researchers treated the mice with broad-spectrum antibiotics for 20 days. After that, the bacterial species that re-colonized the mice’s guts were quite different in their composition from the bacterial species that originally inhabited them.



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