BMJ Open Diabetes Research & Care is an open access journal committed to publishing high-quality basic and clinical research articles regarding type 1 and type 2 diabetes and associated complications. Submissions are subject to rigorous external peer review to Help me with my homework research Diabetes papers good thesis statement for smoking essay. Sample thesis of computer science, attorney cover letter referral. Sample cover letter for recruitment officer job. Popular term paper writers site for masters, nurse informatics resume, professional application letter writer for hire usa! A research paper introduction plays a big role in the research paper, roughly %. Here, the writer makes us aware of the purpose of the research. Without a research paper introduction, your readers are but lost sheep, leave alone them even reading your paper to the end
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Try out PMC Labs and tell us what you think. Learn More. Turmeric Curcuma longaresearch paper for diabetes, a rhizomatous herbaceous perennial plant of the ginger family, research paper for diabetes, has been used for the treatment of diabetes in Ayurvedic and traditional Chinese medicine. The active component of turmeric, curcumin, has caught attention as a potential treatment for diabetes and its complications primarily because it is a relatively safe and inexpensive drug that reduces glycemia and hyperlipidemia in rodent models of diabetes.
Here, we review the recent literature on the applications of curcumin for glycemia and diabetes-related liver disorders, adipocyte dysfunction, neuropathy, nephropathy, vascular diseases, pancreatic disorders, and other complications, and we also discuss its antioxidant and anti-inflammatory properties. The applications of additional curcuminoid compounds for diabetes prevention and treatment are also included in this paper. Natural products have received considerable attention for the management of diabetes and its complications [ 1 — 3 ] which have reached epidemic levels worldwide [ 4 ].
Research paper for diabetes spice turmeric, research paper for diabetes, which is derived from the root of the plant Curcuma longahas been described as a treatment for research paper for diabetes in Ayurvedic [ 5 ] and traditional Chinese medicine for thousands of years Figure 1. Turmeric, research paper for diabetes, curcumin and its chemical structure.
a The root of turmeric. research paper for diabetes Crystallized powder of curcumin. Curcumin is thought to be the main active ingredient derived from the root of turmeric. c The enol and keto forms of curcumin are common structures of the drug. The enol form is more energetically stable in the solid phase and in solution [ 6 ].
The most active component of turmeric, curcumin, has caught scientific attention as a potential therapeutic agent in experimental diabetes and for the treatment of the complications of diabetes patients [ 7 ], primarily because it is effective in reducing glycemia and hyperlipidemia in rodent models and is relatively inexpensive and safe [ 8 — 10 ]. The structure of curcumin Figure 1 cshown to be a diferuloylmethane, was resolved by Lampe and Milobedeska in [ 11 ]. The first paper that described an effect of curcumin related to diabetes described a blood glucose lowering effect of the drug in one diabetic individual only and was published in [ 12 ].
Curcumin has been since extensively studied in experimental animal models of diabetes and in a few clinical trials of type 2 diabetic patients to treat their complications [ 13 ]. This review seeks to briefly summarize the ample scientific literatures regarding curcumin as a potential treatment for diabetes and its associated complications.
Particular attention will be given to the anti-inflammatory and antioxidant properties of curcumin. Since Srinivasan discovered that curcumin has research paper for diabetes effect on glycemia in one patient, a lot of papers have been published to discuss the ability of curcumin in controlling blood glucose in various rodent models Table 1. The most used animal in studying the effect of curcumin is the rat. Various diabetic rat models were employed to probe the effect of curcumin on glycemia.
Dietary curcumin 0. Diabetic mice models were also employed to research paper for diabetes the effect of curcumin on glycemia. In type 2 diabetic KK-A y mice, dietary turmeric extract 0.
The possible mechanisms of the effect of curcumin on glycemia in diabetes models may be explained as follows. First, curcumin could attenuate tumor necrosis factor- α TNF- α levels [ 32 ] and plasma free fatty acids FFA [ 26 ]. It also inhibits nuclear factor-kappa B NF- κ B activation [ 21 ] and protein carbonyl [ 34 ], lipid peroxidation [ 32 ], and lysosomal enzyme activities N-acetyl- β -d-glucosaminidase, β -d-glucuronidase, β -d-galactosidase [ 27 ].
In addition, curcumin can decrease the levels of thiobarbituric acid reactive substances TBARS and the activity of sorbitol dehydrogenase SDH [ 152435 ]. Second, curcumin has the ability of induction of peroxisome proliferator-activated receptor-gamma PPAR- γ activation [ 28 ], research paper for diabetes. Curcumin also can elevate plasma insulin level and increase lipoprotein lipase LPL activity [ 30 ].
Third, curcumin is involved in activating of enzymes in liver, which are associated with glycolysis, gluconeogenic, research paper for diabetes, and lipid metabolic process [ 30 ], and activating nuclear factor erythroidrelated factor-2 Nrf2 function as well [ 33 ], research paper for diabetes.
Further, curcumin supplemented with vitamin C [ 20 ], yoghurt [ 36 ], and bone marrow transplantation [ 32 ] was effective in reducing the levels of blood glucose, Hb, and HbA1C in STZ diabetes models. However, several researchers claimed that curcumin has no significant effect on blood glucose.
The reason for yielding conflicting results from different groups may be due research paper for diabetes different induction diabetes rodent models or different administration of curcumin. Diabetic patients often suffer from fatty liver disease and other liver disorders [ 39 ].
Babu and Srinivasan [ 40 ] found that STZ-induced diabetic rats fed dietary curcumin for 8 weeks excreted less albumin, urea, creatine, and inorganic phosphorus. Curcumin also reduced liver weight and lipid peroxidation products in the plasma and urine. In this study the beneficial effects of curcumin occurred independently of changes in glycemia or body weight. A further study by this group [ 41 ] suggested that hepatic cholesterol-7a-hydroxylase mediates the hypolipidemic action of curcumin in STZ diabetic rats.
The effect of curcumin on lipidemia was also demonstrated by other groups [ 16 research paper for diabetes, 202536 ]. In sodium arsenite induced liver disorder rats, research paper for diabetes, oral administration of curcumin can decrease total lipid, cholesterol, triglyceride TGand low density lipoprotein-cholesterol LDL-c [ 31 ].
Improved lipidemia by curcumin may be attributed to the induction of PPAR- γ activity [ 2842 ] that is linked to adipogenesis [ 43 ]. This improvement may also implicate the normalization of enzymatic activities [ 30 ] involved in lipid peroxidation [ 25 ] and glucose metabolism, including antioxidant enzymes superoxide dismutase and catalase SODC and glutathione peroxidase GPxhepatic glucose regulating enzymes glucosephosphatase G6Pasephosphoenolpyruvate carboxykinase PEPCKhepatic lipid regulating enzymes fatty acid synthase, 3-hydroxymethylglutaryl coenzyme reductase, research paper for diabetes, and acyl-CoA: cholesterol acyltransferase [ 36 ], and malondialdehyde MDA [ 2238 ].
AMP-activated protein kinase AMPK is a strong energy regulator that controls whole-body glucose homeostasis in the liver and other key tissues in type 2 diabetes [ 44 ].
AMPK could stimulate glucose uptake and mediate suppression of hepatic gluconeogenesis. G6Pase and PEPCK are key enzymes involved in hepatic gluconeogenesis in the liver.
Increased expression of G6Pase and PEPCK may have deleterious effects in diet-induced insulin resistance and type 2 diabetes [ 45 ]. Kim et al. They further demonstrated that curcumin could increase phosphorylation of AMPK [ 47 ] and its downstream target acetyl-CoA carboxylase ACC [ 9 ] in H4IIE and Hep3B cells.
Hyperleptinemia associated with type 2 diabetes could cause hepatic fibrosis, which activates hepatic stellate cells HSCs. As a sensor of cellular energy homeostasis, AMPK also stimulates fatty acid oxidation and regulates lipogenesis. Curcumin-mediated activation of AMPK could inactivate HSCs because of reduced stimulation by leptin [ 48 ], insulin, hyperglycemia [ 49 ], advanced glycation endproducts AGEs [ 50 ], and oxidized low-density lipoprotein ox-LDL [ 51 ].
The driving mechanisms behind hypolipidemia may be understood as follows. First, curcumin could disrupt insulin signaling and attenuate oxidative stress [ 52 ]. Second, curcumin could suppress membrane translocation and GLUT2-mediated gene expression. Third, curcumin was also able to increase expression of the AGE receptor [ 50 ], research paper for diabetes, and reduce expression of lectin-like oxidized LDL receptor-1 LOX-1 [ 51 ], research paper for diabetes.
In addition, interruption of Wnt signaling [ 53 ] and stimulation of PPAR- γ activity [ 54 ] by curcumin can increase expression of genes involved in lipid accumulation.
Curcumin prevented liver fat accumulation in HFD rats. The anti-inflammatory and antilipolytic properties of curcumin may account for these results, as evident by reduced levels of TNF- α [ 55 ] and plasma FFA [ 26 ].
Further, curcumin normalized increased serum fetuin-A levels in HFD fed rats [ 56 ], while fetuin-A positively contributed to insulin resistance and fatty liver [ 5758 ]. Adipose tissue plays an important role in controlling wholebody glucose homeostasis [ 60 ]. Development of type 2 diabetes may involve deregulation of adiponectin secretion.
Recent studies revealed that curcumin stimulated human adipocyte differentiation [ 7 ] and suppressed macrophage accumulation or activation in adipose tissue [ 61 ] by regulating adiponectin secretion [ 2962 ]. The mechanism may be due to suppression of NF- κ B activation [ 63 ], which reduces TNF- α and nitric oxide NO and inhibits the release of monocyte chemotactic protein-1 MCP-1 from 3T3-L1 adipocytes [ 61 ].
As is known to us, c-Myc and cyclin D1, well-known downstream target genes of β -catenin [ 65 ] [ 66 ], research paper for diabetes, were shown to prevent adipogenesis [ 6768 ]. Diabetic neuropathy is neuropathic disorders that are associated with DM. These conditions are thought to result from diabetic microvascular injury, elevated AGEs, and activated protein kinase C PKC [ 69 ], research paper for diabetes.
Curcumin has been actively involved in modulating the diabetic neuropathic disorders by the following lines of evidence. Curcumin effectively suppressed the development of diabetic cataracts in rat models of STZ-induced diabetes by reversing changes in lipid peroxidation, reduced glutathione, research paper for diabetes, protein carbonyl content, and activities of antioxidant enzymes, which is beneficial to normalize expression of α A-crystallin and α B-crystallin [ 7071 ].
An increased expression of α A-crystallin and decreased expression of α B-crystallin were contributed to the reduction hydrophobicity and altered secondary and tertiary structures of acrystallin, which resulted in loss of neuroprotective function in diabetes [ 7273 ].
Suryanarayana et al. Further, hyperglycemia-induced aggregation and insolubilization of lens proteins were also prevented by curcumin. Premanand et al. Curcumin may modulate antioxidant factors, including oxidatively modified DNA 8-OHdGSODC, glutathione [ 77 ], and inflammatory parameters, including TNF- αIL-1 βVEGF [ 78 ], and NF- κ B [ 79 ], and may also inhibit activation of nucleotide excision repair enzymes [ 80 ] in the retina of STZ-induced diabetic rats.
In addition, curcumin has been show to attenuate diabetes-induced cognitive deficits, as measured by the Morris water maze test [ 81 ], and cholinergic dysfunction involving acetylcholinesterase activity and cholinergic receptors [ 1782 ] through regulation of GLUT3, dopamine D1, D2 receptors, CREB, phospholipase C [ 83 ], and insulin receptors [ 84 ]. These changes may be in part due to decreased glutamate-mediated excitotoxicity by curcumin, research paper for diabetes, which alters the neurochemical parameters NMDA and AMPA receptors [ 85 ] in the cerebral cortices of diabetic rats.
Curcumin reduced expression of single-minded 2 Sim2 [ 86 ], which is involved in hyperglycemia-induced neuronal injury and impairment of learning and memory. Curcumin-mediated suppression of β -amyloid oligomers induces phosphorylation of tau and degradation of insulin receptor substrate via c-Jun N-terminal kinase JNK signaling in cultured hippocampal neurons, which is beneficial to improve cognitive deficits and insulin signaling in Alzheimer's disease [ 87 ], research paper for diabetes.
By virtue of its antioxidant and anti-inflammatory properties, the neuroprotective effects of curcumin are marked by alterations in MDA, total oxidant status, total antioxidant status, oxidative stress index, and NO [ 91 ] levels in the brain and sciatic tissues research paper for diabetes diabetic rats [ 8192 ], which are mediated through regulation of TNF- α and TNF- α receptor [ 818990 ].
Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria, progressive decline in the glomerular filtration rate, and elevated arterial blood pressure [ 93 ]. Currently, research paper for diabetes, diabetic nephropathy is the leading cause of chronic kidney disease [ 94 ] and one of the most significant long-term complications in terms of morbidity and mortality for individual patients with diabetes.
There are multiple mechanisms by which curcumin may ameliorate renal damage. Curcumin increases blood urea nitrogen [ 21research paper for diabetes ] and promotes clearance of creatine and urea [ 1696 ]. In addition, curcumin decreases levels of albuminuria [ 3676 ] and enzymuria, including levels of N-acetyl-D-glucosaminidase, lactate dehydrogenase LDHaspartate aminotransferase, alanine aminotransferase, and alkaline and acid phosphatases.
A further study revealed that curcumin induces changes in posttranslational modification of histone H3 and altered expression of HSP and p38 mitogen-activated protein kinase MAPK in diabetic kidneys [ 95 ]. These changes were mediated through inhibition of p and NF- κ B [ 98 ]. In addition, research paper for diabetes, Ma et al.
These mechanisms may be due to curcumin-mediated activation of AMP [ ], which reduced expression of VEGF [ ] and VEGF receptor, diminished the activities of PKC- α and PKC- β 1 [ 23 ] and suppressed sterol regulatory element-binding protein SREBP -1c [ ].
Clinical trials further confirmed the effect of curcumin on end-stage renal disease and showed that curcumin reduced transforming growth factor- β TGF- βIL-8, and urinary protein levels [ ]. Vascular disease is a common long-term complication of diabetes. Diabetic vascular disease causes damage to large and small blood vessels throughout the research paper for diabetes. Curcumin has been reported to be active against research paper for diabetes vascular disease demonstrated by the following list of lines of evidence.
First, curcumin modulated PKC- αPKC- β 2, and MAPK [ ] and inhibited p [ ] in experimental diabetic cardiomyopathy. Second, curcumin suppressed accelerated accumulation of AGE collagen and cross-linking research paper for diabetes collagen in the tail tendon and skin of diabetic rats [ ]. These effects were mediated by inhibition of VEGF [ ], NF- κ B, and AP-1 [ ]. Third, curcumin reduced endothelial nitric oxide synthase eNOS and inducible nitric oxide synthase iNOS levels, leading to less oxidative DNA and protein damage.
This effect was also mediated by NF- κ B and AP-1 in diabetic rat hearts and microvascular endothelial cells stimulated with high glucose [].
Inside the Diabetes Research Institute's Lab
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BMJ Open Diabetes Research & Care is an open access journal committed to publishing high-quality basic and clinical research articles regarding type 1 and type 2 diabetes and associated complications. Submissions are subject to rigorous external peer review to HOW TO START (AND COMPLETE) A RESEARCH PAPER. You are a re-entry student and it's been fourteen years since you've written a paper. You coasted through high school on your charm and good looks and never actually wrote a research paper. You have written research papers, but every time is like the first time, and the first time was like a root canal Nov 24, · The first paper that described an effect of curcumin related to diabetes described a blood glucose lowering effect of the drug in one diabetic individual only and was published in Curcumin has been since extensively studied in experimental animal models of diabetes and in a few clinical trials of type 2 diabetic patients to treat their
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