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Are you experiencing few symptoms like sudden fatigue, blurry vision, dehydration, excessive thirst and stubborn wounds? Also called as Gestational Diabetes Mellitus (GDM), Gestational Diabetes is a condition that usually affects women during pregnancy. Diabetes is an alarming problem as it may lead to loss of vision, kidney cancer or kidney failure and foot problems. Diabetes has gripped the world with its far-reaching consequences on the health of an individual.
Type 2 Diabetes is a very common metabolic disorder that leads to the relative ineffectiveness and manufacture of insulin. Diabetes mellitus is a medical condition where the body is unable to control the level of blood sugar. Diabetes in middle aged women is the most common form of diabetes and it is known as type 2 diabetes. Science, Technology and Medicine open access publisher.Publish, read and share novel research. 1995 Isolation and structural identification of 1,25-dihydroxyvitamin D3 produced by cultured alveolar macrophages in sarcoidosis. 1983 Metabolism of 25-hydroxyvitamin D3 by cultured pulmonary alveolar macrophages in sarcoidosis. 2003 Tolerogenic dendritic cells induced by vitamin D receptor ligands enhance regulatory T cells inhibiting autoimmune diabetes. 2010 Glycemic changes after vitamin D supplementation in patients with type 1 diabetes mellitus and vitamin D deficiency.
2009 Genome-wide association study and a meta-analysis find that over 40 loci affect risk of type 1 diabetes. 1983 Specific high-affinity receptors for 1,25 dihydroxyvitamin D3 in human peripheral mononuclear cells: Presence in monocytes and induction in T lymphocytes following activation. 1995 Susceptibility to human type 1 diabetes at IDDM2 is determined by tandem repeat variation at the insulin gene mini satellite locus. 1994 A polymorphic locus near the insulin gene is associated with insulin-dependent diabetes mellitus. 2001 1alpha,25-Dihydroxyvitamin D3 has a direct effect on naive CD4+ T cells to enhance the development of Th2 cells. 1996 1,25-dihydroxyvitamin D3 reversibly blocks the progressions of relapsing encephalomyelitis, a model of multiple sclerosis. 1998 1,25-dihydroxyvitamin D3 prevents and ameliorates symptoms in two experimental models of human arthritis. 1998 1,25-dihydroxy-vitamin D3 restores sensitivity to cyclophosphamide-induced apoptosis in non-obese diabetic (NOD) mice and protects against diabetes. 1998 Prevention of autoimmune destruction of syngeneic islet grafts in spontaneously diabetic nonobese diabetic mice by a combination of a vitamin D3 analog and cyclosporine.
2000 Vitamin D receptor gene polymorphisms influence susceptibility to type 1 diabetes mellitus in the Taiwanese population. 1998 Prevention of type 1 diabetes in nonobese diabetic mice by late intervention with nonhyperclcemic analogs of 1,25-dihydroxyvitamin D3 in combination with a short induction course of cyclosporine A. 1997 The nonobese diabetic mouse as a model of autoimmune diabetes: Immune dysregulation gets the NOD. 1998 Inhibition of IL12 production by 1,25-dihydroxyvitamin D3: involvement of NF-?B down regulation by 1,25-dihydroxy vitamin D3. In the pathogenesis of type 1 diabetes, HLA class II molecules on the surface of antigen-presenting cells (APCs) present fragments of pancreatic -cell proteins to a subclass of T cells called T helper (Th) cells. Until now the exact mechanism of insulin secretion failure in type 2 diabetes has not been completely understood. Type 2 diabetes occurs when insulin production from pancreatic beta cells either fails, or peripheral tissues become resistant to the hormone insulin preventing the uptake of glucose from the blood stream into cells for fuel. Designing new treatment options for type 2 diabetes has been difficult considering the exact mechanism of insulin secretion was not understood.
To test the importance of Snapin in insulin secretion a drug which inhibits its production was added. These exciting new findings will not only propel diabetic research but also help develop more accurate treatment options.
People with type 1 diabetes CANNOT cordupe insulin which brings the blood sugar down so just about everything they eat causes their blood sugar to rise. The popularity of coconut oil has increased dramatically, particularly after TV personality Dr. Miraculous health claims about any food or nutrient need to be looked at closely, and considered in terms of the what peer-reviewed studies indicate. Coconut oil is much higher in saturated fat than most other sources of fats and oils in our diet, which is why it is solid at room temperature. It is the very high percentage of saturated fat that is in Coconut oil that is concerning to many health care professionals, as saturated fats in general have been associated with an increase in “bad” cholesterol levels (LDL). Coconut Oil is high in what is called “Medium Chain Triglycerides” or “MCTs” which are metabolized differently than the longer chain fats – going straight to the liver, rather than needing to be broken down through digestion. A quarter (~24%) to a third (33%) of the fatty acids in Coconut Oil contain the long-chain saturated fats, including Mysteric (13-19 %) and Palmitic Acids (8-11%) and ~10-20% of the fatty acids are made up of 2 short chain saturated fatty acids, Caproic (Decoic) Acid (5-9%) and Caprylic Acid (6-10%). The remaining 10% of the fatty acids are unsaturated, mostly Oleic Acid with a small amount of Linoleic Acid.
Some weight-loss studies using 100% medium chain triglycerides have shown modest weight loss compared to the use of olive oil over a 4-month period, however a study comparing Coconut oil (~50% MCTs) with soy bean oil (almost all long chain triglycerides), did not have a significant impact on weight loss over a 3-month period. When it comes to cholesterol, there are numerous studies that have found that coconut oil raises HDL, the so-called “good cholesterol”, to a greater extent than olive oil however, some studies indicated that coconut oil increases LDL (the “bad cholesterol”), whereas other studies have found that it doesn’t change LDL cholesterol, or if it did raise it, it was in an insignificant amount. While it is approximately half MCT oil which may help lower abdominal fat, still ~40% of Coconut Oil is long chain saturated fat, which may impact heart health.
Introduction: New Year celebrations have come and gone and by now the reality of our ambitious New Year resolutions has set in. The reality is that only 8% of people are actually successful in achieving their New Year’s resolutions — so what makes them successful? The key to success is to pursue a goal that focuses on the positive but targets a specific outcome that is attainable. A goal is a mental representation of a positive outcome that one commits to and setting goals creates sense of urgency and motivation that would seem to provide all that’s needed to accomplish the desired outcome. To achieve success in accomplishing goals requires setting ones that have a clear objective, are specific and that has an outcome that can be measured. When creating a plan, make sure to determine a clear objective and focus in on a specific goal which will help keep you motivated and on track rather than feeling overwhelmed. This can be difficult for many as majority of people tend to bite off more than they can chew. This is where you need to assess your capabilities and skills. Give yourself a period of time or a specific time frame during which the goal will be attained. Celebrate your success no matter how small it is; every small step in the right direction gets you closer to your goal and further away from where you were.
For more information on how we can help, please click on the Contact Us tab above and send us a note. Norcross, JC et al, Auld lang syne: success predictors, change processes, and self-reported outcomes of New Year’s resolvers and nonresolvers. If you or a family member want to see Aman for clinical service in English or Punjabi, please click the Contact Us tab above and send her a note!
IntroductionThis chapter will review the role of vitamin D in the pathogenesis and treatment of type 1 diabetes mellitus.
Vitamin D supplement in early childhood and risk for type 1 (insulin-dependent) diabetes mellitus. In turn, the autoreactive Th cells stimulate cytotoxic T cells (CTLs) to attack insulin-producing -cells (); HLA class I proteins on the -cell surface present -cell peptides to CTLs.

Johns Hopkins researchers believe they have uncovered the molecular switch for insulin secretion. Snapin is a protein  produced in nerve cells and plays an important role in cell communication, and has also been found in pancreatic beta cells.
Oz made claims that coconut oil can help people lose weight, treat skin conditions and help ulcers.
Approximately 90% of the fat in coconut oil is saturated fat, compared with only 63% for butter, for example.
What makes Coconut Oil different than other oils is that half of the saturated fatty acid in it are made up of a Medium Chain Triglyceride, called Lauric Acid (44 – 52%). While the actual amount of weight loss with MCT oil may not be substantial, studies seem to indicate that it is “visceral adiposity” or “belly fat” that decreases, lowering waist circumference. Increase is LDL cholesterol is a concern as it is associated with an increase risk of heart disease. While Coconut Oil has been found to increase HDL (“good” cholesterol), it may raise LDL cholesterol (or may not) , but like any fat, Coconut Oil has a lot of calories. People with a risk of heart disease should be cautious about increasing their intake of coconut oil and would be better looking to cold pressed olive oil which are 65-80% monounsaturated (oleic), 7-16% saturates (palmitic) or using cold pressed avocado oil which are 76% monounsaturated (oleic and palmitoleic acids), 12% polyunsaturates (linoleic and linolenic acids) and only 12% saturates (palmitic and stearic acids). An Open-Label Pilot Study to Assess the Efficacy and Safety of Virgin Coconut Oil in Reducing Visceral Adiposity. The difficulty lies in that although one might value the positive outcome associated with the goal (such as being healthy), without a definable goal there is a lack of direction with respect to the specific types of behaviour change needed to accomplish it. It  needs to provide direction with regards to what we are going to do; specifically what action we are going to take. In order to be successful with your goal, it’s important to set a goal that is actually attainable. Taking on too many goals makes achieving all of them more difficult and increases the likelihood of getting discouraged.
You don’t want to track it too often as it takes time to see results but don’t take too long either as you might need to adjust your goal along the way.
Plan for success yet be prepared for obstacles that could make it hard to achieve your goals.
Her ability to adapt favourite Punjabi foods and make them accessible to those in the South Asian community that need to control their blood sugar or lower their cholesterol results in her being in high demand!
The activation of the T-cell by various stimuli (antigens), is brought by major histocompatibility complex (MHC-HLA II). At the level of the antigen-presenting cell (such as dendritic cells; DCs), 1?,25(OH)2D3 inhibits the surface expression of MHC class II-complexed antigen and of co-stimulatory molecules, in addition to production of the cytokine IL-12, thereby indirectly shifting the polarization of T cells from a Th1 towards a Th2 phenotype.
JOD is a lifelong disease and will require daily insulin injections and constant monitoring of both blood and urine. Th cells also stimulate B cells to produce antibodies against cells of the islets of Langerhans.
Summary of Health Canada’s Assessment of a Health Claim about the Replacement of Saturated Fat with Mono- and Polyunsaturated Fat and Blood Cholesterol Lowering. They also need to be realistic and have a time frame in which the goal is to be accomplished. Then create a plan that you can commit to working towards so that you don’t lose confidence because it’s beyond your capabilities. This figure shows also, inhibitors of T-cell activation: cytotoxic T lymphocyte antigen 4 (CTLA-4) and lymphoid tyrosine phosphatase (LYP). In addition, 1?,25(OH)2D3 has immunomodulatory effects directly at the level of the T cell, by inhibiting the production of the Th1 cytokines IL-2 and IFN-? and stimulating the production of Th2 cytokines. We will summarize the results of in-vitro and animal studies and will conclude with a review of the relevant clinical trials.2. Moreover, KIR receptors on natural killer cells (NK) can also engage with HLA class I proteins on the islet cells and, depending on the type of KIR, help to activate or inhibit autoimmune responses against -cells.
DefinitionType 1 diabetes mellitus is an autoimmune disease in which the pancreas is unable to respond to secretagogue stimulation with appropriate insulin secretion. Both Th2 and Tregs can inhibit Th1 cells through the production of counteracting or inhibitory cytokines. Hyperglycemia develops when more than 70-90% of the insulin-producing beta cells are destroyed. Together, these immunomodulatory effects of 1?,25(OH)2D3 can lead to the protection of target tissues, such as ? cells, in autoimmune diseases and transplantation. An autoimmune destructive process, which plays a central role in the development of type 1 diabetes mellitus, is facilitated by the subject’s own genetic susceptibility and by non-genetic factors. Vitamin D deficiency is a non-genetic factor that appears to be associated with an increased risk of developing type 1 diabetes mellitus. The acute complications include life-threatening conditions like severe hypoglycemia or diabetic ketoacidosis (DKA). Chronic diabetic complications can be divided into microvascular complications (retinopathy, neuropathy and nephropathy) and macrovascular complications (cardiovascular, cerebrovascular and peripheral vascular disease).
I can eat an almost unlimited amount of nuts without my blood sugar going over 100 at any point. Severe microvascular and macrovascular complications can lead to renal failure (the most common cause of hemodialysis in the US), blindness or lower extremity amputations.
Rather than using the Glycemic Index, I urge your friend to think about food in terms of carbohydrates. EpidemiologyIn 2010, about 215,000 people younger than 20 years of age had diabetes (type 1 or type 2) in the United States.
He should experiment with different quantities and types of carbohydrates by eating and then testing his blood sugar.
About 27% of those with diabetes (approximately 7 million Americans) do not know they have the disease. He may learn that he’s more tolerant of carbohydrates in the afternoon or evening than the morning. Type 1 diabetes mellitus continues to be highly prevalent in many countries, with an overall annual increase estimated at 3% (International Diabetes Federation [IDF] 2010).
The Glycemic Index simply doesn’t tell us anything except for how some people without diabetes handled carbohydrates. Natural historyThe natural history of type 1 diabetes is characterized by an autoimmune destruction of the beta cells in the islands of Langerhans in the pancreas.
The autoimmune process has cellular and humoral components, leading to the destruction of the beta cells and a decreased insulin secretion. As beta-cell mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels. After 70-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed. In some patients years will go by before the onset of diabetes, while other patients may never develop beta cell insufficiency, perhaps due to the regaining of tolerance. Most patients with type 1 diabetes mellitus have one or more susceptible human leukocyte antigen (HLA) class II, and over 90% have beta cell autoantibodies present. The appearance of circulating islet cell autoantibodies is the first detectable sign of this immune process.4. However, extra-genetic components influence the penetrance of diabetes susceptibility genes. If data are obtained at a single point in time, the risk of type 1 diabetes mellitus between monozygotic twins can be as low as 30%, but if the monozygotic twins are followed long-term, the cumulative incidence of diabetes reaches 65% (Redondo et al., 2008).
In the same cohort of monozygotic twins, the rate of persistent autoantibody positivity, type 1 diabetes mellitus, or both, reached 78% (Redondo et al., 2008). To better understand the genetic susceptibility to diabetes, candidate gene studies were conducted in order to identify genes that are associated with autoimmune type 1 diabetes.Human leukocyte antigen (HLA) associations have been long recognized in many autoimmune diseases. In type 1 diabetes mellitus, the HLA on chromosome 6p21 is well described and is considered to play an important role in more than 50% of the familial cases in Caucasians (Noble et al., 1996).

HLA DR4-DQ8 or DR3-DQ2 haplotypes are detected in up to 90% of patients with type 1 diabetes mellitus (Devendra & Eisenbarth, 2003). First-degree relatives of the patients who carry the highest risk haplotype combination also have a higher risk of developing diabetes mellitus as compared to the relatives of diabetes patients who do not have this haplotype and who develop type 1 diabetes mellitus later in life (Gillespie et al., 2002).
Another HLA haplotype (DR15-DQ6) might have protective properties, and is found in a much larger percentage in the general population (20%) as compared to less than 1% in patients with type 1 diabetes mellitus (Eisenbarth & Gottlieb, 2004).
Glutamic acid decarboxylase (GAD) antibodies are more frequent in patients with HLA DR3-DQ2, whereas insulin auto-antibodies (IAA) and protein tyrosine phosphatase-like protein antibodies (IA-2 antibodies) are more frequent in patients with HLA DR4-DQ8. The insulin gene contributes 10% to the genetic susceptibility in developing autoimmune diabetes (Bell et al., 1984).
The risk of developing diabetes depends on the expression of the insulin protein in the thymus which can cause a defective central tolerance to the insulin molecule. T cells are recognized to be a major part of the immune process in diabetes mellitus, and several genes involved in T cell regulation are associated with type 1 diabetes mellitus.
Autoimmune processOne of the best animal models for type 1 diabetes mellitus is the nonobese diabetic mouse (NOD).
NOD mouse develops type 1 diabetes mellitus spontaneously, over the course of a few months, allowing the investigators to study this process stage by stage. Many reports describe in detail the genetics, the immune process, the influence of the environment and most importantly, the potential therapies to prevent, delay or reverse the destructive process that leads to type 1 diabetes mellitus in this model. Delovitch and Singh (Delovitch & Singh, 1997) reviewed the use of NOD mouse in the studies of type 1 diabetes mellitus. In NOD mice, the first step is the infiltration of the peri-islet regions of the pancreatic islets by dendritic cells (DC) and macrophages, followed by T cells (CD4+ and CD8+). It is followed by a slower, progressive T cell destruction of the beta cells (insulitis), by 4-6 months of age (Delovitch & Singh, 1997). Thus, the T cells and the dendritic cells are key players in the immune process leading to type 1 diabetes mellitus.The dendritic cells (DC) are antigen-presenting cells which originate from the bone marrow. After infiltrating the pancreas and undergoing antigenic maturation, DC secrete IL-12 and present the processed antigen (on their surface and in association with the major histocompatibility complex [MHC] class II) to other cells of the immune system (i.e. T cells) (see Fig 1).T cells are categorized mainly based on their immune actions, achieved via the different cytokines they secrete. T helper 2 cells (Th2) are important in humoral immunity (activate B cells and antibody production, down regulating Th 1 cells) and secrete type 2 cytokines: interleukins 4, 5, 6, 9 and 10 (Rabinovitch, 1998) (Fig.
They have an inhibitory effect on the Th1 cells, which are destructive to the pancreatic beta cells.
In the NOD mouse, it appears that the immunologic self-tolerance to pancreatic beta cells is lost. The disruption of the equilibrium between Th1 and Th2 cells in the thymus and in the periphery is believed to play a crucial role in the pathogenesis of autoimmune diabetes mellitus (Delovitch & Singh, 1997). Once Th1 cells are produced they will secrete interferon ? (IFN ?) and IL-2, leading to the activation of macrophages and cytotoxic T cells, which are destructive to the pancreatic beta cells (Adorini, 2001).
The same Th1 cells will stimulate the IgG2a autoantibodies against the islet beta cells autoantigens (Delovitch & Singh, 1997). Autoimmune diabetes can be transferred from a diabetic NOD mouse to an unaffected mouse via T cells (Bendelac et al., 1987).
NOD mice develop a spontaneous loss of T-cell tolerance to glutamic acid decarboxylase antibodies (GAD), leading to autoimmune diabetes (Kaufman et al., 1993). Exposure to glutamic acid decarboxylase (GAD65 and GAD67) led to an increased T cell proliferation as early as 4 weeks of life in NOD mice, coinciding with the onset of insulitis (Tisch 1993). Some of the other beta-cell antigens elicited an increased immune response after a few more weeks, but there were other beta-cell antigens that did not trigger an immune reaction (for example, amylin) (Tisch 1993). To further support the central role of GAD antigen in autoimmune diabetes, the beta-cell-specific suppression of GAD expression in antisense GAD transgenic NOD mice was demonstrated to prevent the production of diabetogenic T cells and the onset of diabetes (Yoon et al., 1999) In humans, the pancreas becomes infiltrated with mononuclear cells.
Autoantibodies to insulin (IAA), glutamic acid decarboxylase (GAD) and insulinoma associated-2 antibody (IA-2) are demonstrated years before the clinical symptoms of diabetes.
The presence of autoantibodies alone does not explain the development of diabetes, since it is recognized now that children born to type 1 diabetic mother with high antibody titers transferred through the umbilical cord do not develop diabetes more often than expected. Environmental component The environment is implicated in the pathogenesis of type 1 diabetes mellitus by many studies.
Environmental factors have an important role in initiating an immune process that ultimately leads to pancreatic beta cell destruction and clinically apparent diabetes mellitus.
Many environmental factors have been proposed, including viruses (rubella, mumps or coxsackievirus B4), toxic substances and cytotoxins.
Before the eradication of rubella in most countries, congenital rubella was strongly associated with the development of type 1 diabetes mellitus (Menser et al., 1978). A recent meta analysis of observational studies has shown an association between type 1 diabetes and enterovirus infection (Yeung 2011). While some theories implicate viral infections in the pathogenesis of type 1 diabetes, a recent hypothesis argues that a decreased exposure to microbes may contribute to the current increase in autoimmune disease. This theory is known as “the hygiene hypothesis” (Gale, 2002).It is a known fact that the incidence of autoimmune diabetes follows a geographical pattern, with many studies reporting an association between type 1 diabetes and vitamin D status. A few large ecological studies describe a pattern of geographical variation, with an increased incidence of type 1 diabetes in the areas located north of the equator.
Furthermore, seasons appear to also influence the incidence of type 1 diabetes, with the highest incidence during winter and the lowest during summer. Typically, the treatment for type 1 diabetes mellitus involves insulin therapy, but in the last few years new therapies have been approved as well (for example, Symlin).
For newly diagnosed patients with autoimmune diabetes, combination therapy has been suggested in an attempt to minimize beta cell destruction and prolong pancreatic function. The new therapeutic options include: immunotherapy, vaccines, drugs that influence T cell action, anti-inflammatory drugs (for example, one time use of anti-IL-1R drug), or long-term treatment with B cell components to induce regulatory T cells (oral or nasal insulin, insulin peptide therapy, GAD-Alum or the proinsulin DNA vaccines). Glucagon-like peptide 1-related drugs (GLP-1) could be also considered as a therapeutic option because they promote peritubular pancreatic cell growth (Von Herrath, 2010).5.
Vitamin DAlthough initially described as a “vitamin”, vitamin D is now recognized to be a hormone, synthesized in the human body and exerting its action on other organs via a nuclear receptor (vitamin D receptor, VDR). Even though vitamin D can be obtained from the diet in small quantities, the main source of vitamin D is the skin. Under the direct influence of ultra violet B light (UVB light), 7-dehydrocholesterol (DHC) (provitamin D3) is converted into pre-vitamin D3, which is then further converted into cholecalciferol (vitamin D3) via thermal isomerization. Interestingly, if pre-vitamin D3 continues to be exposed to UVB, it will be converted into biologically inactive metabolites (tachysterol and lumisterol), preventing a potential UVB- induced vitamin D intoxication (Holick, 1999) The other source of vitamin D is the diet, which contains cholecalciferol (vitamin D3), originating from animal sources, and ergocalciferol (vitamin D2), deriving from plants (Holick, 1999).Regardless of their source, once they enter into the circulation, forms of inactive vitamin D3 or D2 bind to the vitamin D-binding protein (DBP) and are transported to the liver.
The inactive vitamin D is activated through a 2-step hydroxylation process via two hydroxylases that belong to the cytochrome P450- dependent steroid hydroxylases (CYP450). In the liver, vitamin D undergoes the first hydroxylation at C-25 via some of the CYP 450 vitamin D 25-hydroxylases, forming calcidiol (25-hydroxyvitamin D) (Prosser & Jones, 2004).
The activity of 1?-hydroxylase in the immune cells is not under the regulation of parathyroid hormone and 1?-,25(OH)2D3, but rather under immune cytokine regulation. A defect in the up-regulation of 1?-hydroxylase after immune stimulation is described in NOD mouse (Overbergh et al., 2000). Extrarenal distribution of 1?-hydroxylase becomes important in understanding the extra-skeletal effects of vitamin D.VDR is part of the nuclear receptor super family of ligand-activated transcription factors, which also includes glucocorticoid, thyroid hormone and estrogen receptors. The gene for VDR is located on chromosome 12q12-14, and shows great polymorphism (Haussler et al., 1998). After 1,25 (OH)2D3 binds to VDR, it induces conformational changes that facilitate heterodimerization with the retinoid X receptor and the recruitment of nuclear receptor coactivator proteins, which then act on the chromatin.

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