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Research paper on diabetes

Research paper on diabetes

research paper on diabetes

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Try out PMC Labs and tell us what you think. Learn More. Turmeric Curcuma longaa rhizomatous herbaceous perennial plant of the ginger family, has been used for the treatment of diabetes in Ayurvedic and research paper on diabetes 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, research paper on diabetes, 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 research paper on diabetes received considerable attention for the management of diabetes and its complications [ 1 — 3 ] which have reached epidemic levels worldwide [ 4 ].


The spice turmeric, which is derived from the root research paper on diabetes the plant Curcuma longahas been described as a treatment for diabetes in Ayurvedic [ 5 ] and traditional Chinese medicine for thousands of years Figure 1. Turmeric, curcumin and its chemical structure. a The root of turmeric. b 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 cresearch paper on diabetes, shown 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 an 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 show the effect of curcumin on glycemia. In type research paper on diabetes 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, research paper on diabetes, curcumin has the ability of induction of peroxisome proliferator-activated receptor-gamma PPAR- γ activation [ 28 ], research paper on 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, and lipid metabolic process [ 30 ], and activating nuclear factor erythroidrelated factor-2 Nrf2 function as well [ 33 ].


Further, curcumin supplemented with vitamin C [ 20 ], yoghurt [ 36 ], and bone marrow transplantation [ 32 ] was effective in reducing the levels of blood glucose, Hb, research paper on diabetes, 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 to different induction diabetes rodent models research paper on diabetes 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, research paper on diabetes. In this study the beneficial effects of curcumin occurred independently of changes in glycemia or body weight, research paper on diabetes. 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 [ 16202536 ]. In sodium arsenite induced liver disorder rats, 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 G6Pase research paper on diabetes, phosphoenolpyruvate carboxykinase PEPCKresearch paper on diabetes, hepatic lipid regulating enzymes fatty acid synthase, 3-hydroxymethylglutaryl coenzyme reductase, 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 ], research paper on diabetes. 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.


Research paper on diabetes a sensor of cellular energy homeostasis, research paper on diabetes, 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, research paper on diabetes, hyperglycemia [ 49 ], research paper on diabetes, 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, research paper on diabetes was also able to increase expression of the AGE receptor [ 50 ], and reduce expression of lectin-like oxidized LDL receptor-1 LOX-1 [ 51 ]. 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 ], research paper on diabetes, 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 ], were shown research paper on diabetes prevent adipogenesis [ 67research paper on diabetes, 68 ].


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 on 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, 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 research paper on diabetes. These changes may be in part due to decreased glutamate-mediated excitotoxicity by curcumin, which research paper on diabetes 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 research paper on diabetes 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 ].


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 of diabetic rats [ 81research paper on diabetes, 92 ], 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, diabetic nephropathy is the leading cause of chronic kidney disease [ 94 ] and one of the research paper on diabetes significant long-term complications in terms of morbidity and mortality for individual patients with diabetes. There are multiple mechanisms by which curcumin research paper on diabetes ameliorate renal damage. Curcumin increases blood urea nitrogen [ 2195 ] 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, 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 body.


Curcumin has been reported to be active against diabetic vascular disease demonstrated by the following list of lines of evidence, research paper on diabetes. 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 of 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 [research paper on diabetes, ].




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research paper on diabetes

In a paper published in the journal Diabetes, Dr. Brayman and a team of researchers reported exciting findings related to this approach. They found that supplementing IgM obtained from healthy mice into mice with type 1 diabetes selectively reduced the amount of autoreactive immune cells known to target beta-cells for destruction 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 Apr 12,  · A health research paper is an assignment essay given to students to gauge their level of understanding of what they have been taught. Writing such a paper can be quite hectic as it first consumes much time. The research work that is involved, both field and from written manuals is completely exhausting

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