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These studies suggest that type-1 diabetes is a distinct disease often diagnosed in younger individuals and involves autoimmune destruction of insulin-producing cells, while type-2 diabetes typically affects older adults and is characterized by insulin resistance and relative insulin deficiency.
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Diabetes mellitus is a chronic condition characterized by elevated blood glucose levels. It primarily manifests in two forms: Type-1 diabetes (T1D) and Type-2 diabetes (T2D). While both types share some common features, they differ significantly in their etiology, pathophysiology, and management.
Type-1 diabetes is an autoimmune disorder where the body's immune system attacks and destroys insulin-producing beta cells in the pancreas. This leads to an absolute deficiency of insulin, necessitating lifelong insulin therapy for survival . The onset is typically rapid and occurs in childhood or adolescence, although it can also develop in adults.
Type-2 diabetes, on the other hand, is primarily characterized by insulin resistance, where the body's cells do not respond effectively to insulin. This is often accompanied by a relative insulin deficiency as the disease progresses. T2D is strongly associated with obesity, physical inactivity, and genetic factors, and it usually develops in adults, although increasing rates are seen in younger populations due to rising obesity rates .
The clinical presentation of T1D and T2D can overlap, making initial diagnosis challenging. T1D often presents with acute symptoms such as polyuria, polydipsia, weight loss, and fatigue. In contrast, T2D may develop more insidiously, with patients often being asymptomatic or presenting with complications such as cardiovascular disease at diagnosis .
Both types of diabetes are diagnosed based on elevated blood glucose levels. However, additional tests such as autoantibody screening can help distinguish T1D from T2D. The presence of autoantibodies is indicative of T1D, while their absence, along with markers of insulin resistance, suggests T2D.
There is some genetic overlap between T1D and T2D, with certain genetic regions being associated with both conditions. However, the direction of genetic effects often differs, indicating distinct underlying mechanisms. For example, variants near the GLIS3 gene increase the risk for both T1D and T2D, but most shared genetic signals have opposite effects on the two diseases.
Metabolomic studies have identified distinct metabolic profiles for T1D and T2D. Commonly altered metabolites include glucose, fructose, amino acids, and lipids. These metabolic changes can help in understanding the pathophysiological pathways and developing targeted interventions for each type of diabetes.
Both T1D and T2D increase the risk of cardiovascular diseases due to changes in haemostasis, including altered concentrations of coagulatory proteins, platelet hyperactivation, and endothelial dysfunction. However, the mechanisms and severity of these changes can differ between the two types.
Diabetic neuropathy also presents differently in T1D and T2D. T1D is associated with more severe and progressive nerve damage, characterized by axonal atrophy and paranodal degeneration. In contrast, T2D neuropathy tends to have milder initial functional defects but can still lead to significant nerve fiber loss over time.
While Type-1 and Type-2 diabetes share some common features, they are distinct diseases with different etiologies, pathophysiologies, and clinical presentations. Understanding these differences is crucial for accurate diagnosis, effective management, and the development of targeted therapies.
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