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Type 2 Diabetes, Immunity and Cardiovascular Risk: A Complex RelationshipDaniela Pedicino, Ada Francesca Giglio, Vincenzo Alessandro Galiffa, Francesco Trotta and Giovanna Liuzzo[1] Institute of Cardiology, Catholic University, Rome, Italy1.
The vascular complications of DM are further subdivided into micro vascular (retinopathy, neuropathy, and nephropathy) and macro vascular complications [coronary artery disease (CAD), peripheral arterial disease (PAD), cerebrovascular disease]. The risk of chronic complications increases as a function of the duration of hyperglycemia; they usually become apparent in the second decade of hyperglycemia. Following prominent theories, which are not mutually exclusive, have been proposed to explain how hyperglycemia might lead to the chronic complications of DM. Increased intracellular glucose leads to the formation of advanced glycosylation end products (AGEs) via the nonenzymatic glycosylation of intra and extra cellular proteins.
A fourth theory proposes that hyperglycemia increases the flux through the hexosamine pathway, which generates fructose-6-phosphate, a substrate for O-linked glycosylation and proteoglycan production. Growth factors appear to play an important role in DM-related complications, and their production is increased by most of these proposed pathways. Hyperglycemia leads to increased production of reactive oxygen species or Superoxide in the mitochondria; these compounds may activate all four of the pathways described above. Premature cataracts occur in diabetic patients (Figure-5) and seem to correlate with both the duration of diabetes and the severity of chronic hyperglycemia. Diabetic nephropathy- Diabetic nephropathy (nephropatia diabetica), also known as Kimmelstiel-Wilson syndrome, and intercapillary glomerulonephritis, is a progressive kidney disease, caused by angiopathy of capillaries in the kidney glomeruli, and it is characterized by Nephrotic syndrome and diffuse glomerulosclerosis.
Like other microvascular complications, the pathogenesis of diabetic nephropathy is related to chronic hyperglycemia.The mechanisms by which chronic hyperglycemia leads to End Stage Renal Disease ( ESRD), though incompletely defined, involve the effects of soluble factors (growth factors, angiotensin II, Endothelin, AGEs), hemodynamic alterations in the renal microcirculation (glomerular hyper filtration or hyper perfusion, increased glomerular capillary pressure), and structural changes in the glomerulus (increased extracellular matrix, basement membrane thickening, mesangial expansion, fibrosis). The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus.
Diabetic nerve damage can affect the nerves that are important for penile erection, causing erectile dysfunction .Erectile dysfunction can also be caused by poor blood flow to the penis from diabetic blood vessel disease.
Diabetic neuropathy can also affect nerves to the stomach and intestines, causing nausea, weight loss, diarrhea, and other symptoms of gastroparesis (delayed emptying of food contents from the stomach into the intestines, due to ineffective contraction of the stomach muscles).
Despite advances in the understanding of the metabolic causes of neuropathy, treatments aimed at interrupting these pathological processes have been limited.
As a complication, there is an increased risk of injury to the feet because of loss of sensation. The incidence of gangrene of the feet in diabetics(Figure-6) is 30 times more than that in age-matched controls. Chronic pyogenic infections of the skin may occur, especially in poorly controlled diabetic patients. Schematic representation of the principal mechanisms linking diabetes, vascular injury and atherosclerotic disease.
Nonvascular complications include problems such as gastroparesis, infections, and skin changes. Since type 2 DM often has a long asymptomatic period of hyperglycemia, many individuals with type 2 DM have complications at the time of diagnosis. Among other actions, PKC alters the transcription of genes for fibronectin, type IV collagen, contractile proteins, and extracellular matrix proteins in endothelial cells and neurons. The hexosamine pathway may alter function by glycosylation of proteins such as endothelial nitric oxide synthase or by changes in gene expression of transforming growth factor ? (TGF- ?) or plasminogen activator inhibitor-1 (PAI-1).

Blindness is primarily the result of progressive diabetic retinopathy and clinically significant macular edema. It is due to long standing diabetes mellitus, and is a prime cause for dialysis in many Western countries. Most often, the diagnosis is suspected when a routine urinalysis of a person with diabetes shows too much protein in the urine (proteinuria). As a part of comprehensive diabetes care, microalbuminuria detection, and measurement of the serum creatinine to estimate GFR, should be done at an early stage, when effective therapies can be instituted.
Candidal infection can produce erythema and edema of intertriginous areas below the breasts, in the axillas, and between the fingers. Hyperglycemia induces formation of advanced glycation end products (AGEs) that bind to their receptors (RAGE) present on endothelial cells, smooth muscle cells, monocytes and macrophages, thus promoting vascular inflammation, endothelial dysfunction, and prothrombotic state. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997, 2003)2.
Although hyperglycemia serves as the initial trigger for complications of diabetes, it is still unknown whether the same pathophysiological processes are operative in all complications or whether some pathways predominate in certain organs. Neovascularization of the iris in diabetics can predispose to closed-angle glaucoma, but this is relatively uncommon except after cataract extraction, when growth of new vessels has been known to progress rapidly, involving the angle of the iris and obstructing outflow. An unusual lesion termed necrobiosis lipoidica diabeticorum is usually located over the anterior surfaces of the legs or the dorsal surfaces of the ankles. It causes vulvovaginitis in most chronically uncontrolled diabetic women with persistent glucosuria and is a frequent cause of pruritus.While antifungal creams containing miconazole or clotrimazole offer immediate relief of vulvovaginitis, recurrence is frequent unless glucosuria is reduced. Classification and pathogenesis (Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997)4. RAGE) induces endothelial dysfunction by reducing nitric oxide (NO) release ,  promoting inflammatory reactions, and oxidative stress.
Survival after the onset of ESRD is shorter in the diabetic population compared to nondiabetics with similar clinical features.
Patients should be advised to seek immediate medical care if a diabetic foot ulcer develops.
Improvement in peripheral blood flow with endarterectomy and bypass operations is possible in certain patients. Prevalence of diabetes is higher in western countries because of the increasing of population age, physical inactivity and obesity, however it is rapidly spreading also in developing countries due to the socio-economic growth with progressive urbanization and changes in lifestyle.Cardiovascular disease (CVD) in diabetic patients is characterized by microvascular damage, associated with the development of diabetic retinopathy, nephropathy, and neuropathy, and macrovascular complications linked to the accelerated course of atherosclerosis shown in these patients. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. In some individuals with type 1 diabetes and microalbuminuria of short duration, the microalbuminuria regresses. Both an acute (lasting <12 months) and a chronic form of painful diabetic neuropathy have been described. As diabetic neuropathy progresses, the pain subsides and eventually disappears, but a sensory deficit in the lower extremities persists. Inflammation, diabetes and cardiovascular riskEpidemiological studies conducted at the end of 1970 described diabetes as a major independent risk factor for cardiovascular disease, causing 2-4 folds increase in cardiovascular risk (Kannel & McGee, 1979). Offenbacher, Levels of serum interleukin (IL)-6 and gingival crevicular fluid of IL-1beta and prostaglandin E(2) among non-smoking subjects with gingivitis and type 2 diabetes.

Virmani, 2004Morphologic findings of coronary atherosclerotic plaques in diabetics: apostmortem study.
Several angiographic studies highlighted a greater spread and progression of atherosclerotic disease in diabetes patients. Figure 1.Schematic representation of the principal mechanisms linking diabetes, vascular injury and atherosclerotic disease. Travert, Intensive blood-glucose control and cardiovascular outcomes in patients with type 2 diabetes.
However, the previously described studies have not adequately eliminated potential contamination of the reagents used in the experimental condition with bacterial products. Role of inflammasomes in peripheral insulin resistanceRecent studies also highlighted a crucial role of inflammasomes pathways both in insulin production and in insulin sensitivity.
A first priming step is usually mediated by PRRs, such as TLR, or cytokines receptors known to induce activation of NFkB, and leads to production and intracellular release of inactive forms of NLRP3. IL-1?, produced as a result of inflammasome activation, inhibits insulin signaling (Wen et al., 2011) by direct serine phosphorylation of IRS-1 and induces the expression of TNF-? (Strowig et al, 2012), an insulin-resistance-promoting cytokine as discussed above.
Human ?-cells are capable to produce IL-1? when exposed to elevated glucose concentration (Maedler et al., 2002). Hyperglycemia stimulates mitochondrial ROS production by increasing the activity of the electron transport chain, leading to the activation of NLRP3. Diabetes and adaptive immunityIn the past years, a possible role of adaptive immunity and autoreactive mechanisms in the pathogenesis of T2DM has probably been underestimated and, therefore, poorly investigated. It has been recently demonstrated that T-lymphocytes of patients with T2DM produce large amounts of pro-inflammatory cytokines, such as IL-8, showing in contrast a decreased production of anti-inflammatory cytokines, such as IL-10 (Jagannathan et al., 2010). Another cellular type possibly involved in inflammation and insulin-resistance in T2DM are IL-17 producing T-cells, so called Th17.
In recent years, a higher percentage of a particular T-cell type, CD4+ CD28null T lymphocytes, has been found in diabetic patients undergoing microvascular complications, e.g.
With these premises, the recent finding of an expansion of CD4+ CD28null T-cells in diabetic patients is extremely interesting, suggesting a possible role of adaptive immune disregulation, either primary or induced by the altered metabolic status and the inflammatory environment characterizing the disease, in the increased cardiovascular risk which is one of the most relevant clinical features of T2DM, accounting for the majority of disease-related mortality and morbidity (Giubilato et al., 2011).
Treating T2DM by targeting immunityAs a role of inflammation has been suggested in the development of diabetes and its vascular complications, TLRs and inflammasome could represent attractive drug targets. ConclusionsType 2 diabetes is a complex disease involving the whole metabolic profile of the organism and exerting pathological effects on several organs and systems. The disease is associated with a chronic low-grade inflammation predictive of, and possibly responsible for, many of the clinical signs and complications of T2DM.
The diabetes-associated inflammatory status can be the consequence of the metabolic abnormalities characterizing the disease, but increasing evidences are proposing also an important role of immune system disregulation, involving both innate and adaptive immunity, in the pathogenesis of T2DM.
Hence, any imbalances between them could represent a trigger for metabolic dysfunctions such those related to diabetes.
However, clinical trials have been addressed, with positive results, at evaluating the efficacy of downstream products’ blockers, such as Anakinra, a recombinant IL-1RA.

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