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Diabetes often leads to several undesirable skin conditions that cause skin darkening, rashes, blisters and itching.
These skin conditions may appear to be simple skin problems in the beginning but it can turn into potentially complex issue, if it is left untreated for a long time. Increased sugar content in the blood stream is one of the main causes of skin conditions in diabetes. Insulin resistance occurs when the body fails to respond effectively to the actions of the hormone called insulin. The skin may become dark and appear to be tanned, which may be sometimes misdiagnosed as skin tanning due to over exposure to the sun. Immunity system also forms to be one of the main causes of skin conditions in people with diabetes.
Reduced supply of blood to different parts of the skin also leads to skin condition in people who are suffering from diabetes.
Diabetes is a chronic condition that affects the body's ability to convert sugar into energy. The economic burden of T2D among South Asians makes this an important global clinical and public health challenge. Acanthosis nigricans is probably the most readily recognized skin manifestation of diabetes.
In addition to the direct effects of hyperinsulinemia on keratinocytes, insulin also appears to augment androgen levels in women. Clinically, acanthosis nigricans presents as brown to gray-black papillomatous cutaneous thickening in the flexural areas, including the posterolateral neck, axillae, groin, and abdominal folds. The histopathology of clinical lesions demonstrates papillomatosis and hyperkeratosis but minimal acanthosis. The skin conditions that develop due to diabetes may occur due to various reasons and affect different people in different manner. When the pancreas does not produce enough insulin, the amount of glucose keeps increasing in the blood stream, causing various health problems, including different skin conditions. Pancreas tends to secrete more insulin to compensate for the insulin resistance, causing abnormally increased levels of insulin in the body. But, one of the significant signs of these skin conditions due to insulin resistance includes thick dark patches of skin that mostly appear velvety.
When a person has a background with diabetes in the immediate family, then the chances of developing diabetes skin condition increases. In this chronic ailment, a person’s immune system becomes dysfunctional and begins to attack and destroy the cells that are meant for producing insulin in the body.
These skin conditions occur due to the narrowing of the blood vessels that are responsible for supplying oxygen to the skin. The stress of obesity, combined with a genetically susceptible background, produces insulin resistance and impaired glucose tolerance. This allows sugar (glucose) levels to build up in the blood. Type 2 Diabetes (T2D) is the fifth leading cause of death worldwide, and a major contributor to development of coronary heart disease, stroke, peripheral vascular disease and end-stage renal disease. This non-insulin dependent diabetes mellitus (NIDDM) is primarily characterized by insulin resistance, relative insulin deficiency and hyperglycemia.
Insulin resistance and declined ?-cell function are the core consequences of T2DM (Rhodes et al, 2002). Obesity has also been reported as a major factor in the development of insulin resistance and T2DM (Steinberger et al, 2003). In the first phase of insulin secretion, the level of glucose-stimulated insulin release is impaired in Type 2 diabetes condition and decreased in the second phase (Ward et al., 1986). The Endoplasmic reticulum stress pathway which is active in adipose tissue and liver has a molecular link between obesity, decreased insulin sensitivity and type 2 diabetes.
Many candidate genes and the susceptible loci responsible for Type 2 diabetes mellitus have already been reported and this list is being increased as the research on genetic variation in this metabolic disorder progresses all over the world. The various factors contributing to the development of T2DM have been depicted in Figure 2. Acanthosis nigricans is common in the general population, and most cases are linked to obesity and insulin resistance. High insulin levels stimulate the production of ovarian androgens and ovarian hypertrophy with cystic changes.21 Although associated with elevated androgen levels, the acanthosis nigricans in women with polycystic ovarian syndrome (PCOS) does not respond reliably to antiandrogen therapy, implicating the relative importance of hyperinsulinemia over hyperandrogenism in acanthosis nigricans.


In the majority of cases, the most important factor in diagnosing acanthosis nigricans is recognizing the usually associated hyperinsulinemia, which is a known risk factor for type 2 diabetes. Hyperpigmentation of the basal layer has been variably demonstrated and the brown color of the lesions is attributed to the hyperkeratosis by most.
Topical treatment with calcipotriol,salicylic acid, urea, systemic and topical retinoids have all been used with anecdotal success. It is important to know the causes of diabetic skin conditions, as it helps to understand when just to apply cosmetics to hide the blemishes and when to seek medical help. Vitiligo is one of the most common skin conditions that cause skin discoloration in people with diabetes. In this condition, various skin conditions develop causing thickening and darkening of different parts of the skin.
Most often, genetically susceptive people tend to develop diabetes but this may not be the only reason for developing skin conditions in diabetics.
Due to lack of insulin, the sugar level increases at an abnormal rate in the body and leads to various conditions like skin problems. In this condition, you may notice thickening and discoloration of the toenails, and cold skin. Continued stress, from hyperinsulinaemia, gluco- and lipotoxicity, on the pancreatic-islet -cells results in failure to maintain sufficient insulin levels to compensate for the insulin resistance, leading to elevated glucose levels and the diagnosis of diabetes. Diabetes type 2 is condition where there is low insulin secretion or body is not sensitive to the insulin (not properly utilized by the body) or both. This is considering as a major risk factor for developing diabetes type 2 and other metabolic syndrome. These symptoms occur during blood-glucose rise, and it may disappear when it normalizes.If you have a family history of diabetes or having other diabetes risk factors and feel some of the above symptoms, then immediately, go for a blood test. Liver convert excess glucose in the blood into glycogen and store it for the future requirement. Diabetes develops due to the genetic predisposition and environmental factors, such as improper food-habit, obesity, sedentary lifestyle, urbanization etc. Abnormalities in ?-cell function that results in T2DM include reduced non-glucose insulin secretagogues stimulation, asynchronous insulin release, a decreased conversion of proinsulin to insulin and a significant decrease in ?-cell mass (Mahler et al., 1999).
This endoplasmic reticulum stress in obese individuals leads to suppression of insulin receptor signaling by increased activation of c-Jun N-terminal kinase (JNK) and phosphorylation of insulin receptor substrate–1 (IRS-1) on serine residues (Ozcan et al., 2004). Several drugs have also been reported to cause acanthosis nigricans, including systemic glucocorticoids, nicotinic acid, and estrogens such as diethylstilbestrol. There are many other factors such as damaged immune system and reduced blood flow to different organs that combine together to cause skin conditions in diabetes.
Microvascular complications become apparent over time, depending on how well glucose levels can be controlled.
All diabetes is considering as serious, if not properly treated can lead to dangerous diabetes complications. Diabetes type 1 develops when your body's immune system mistakenly attacks and destroys the insulin-producing cells in the pancreas. I heard from many peoples, who were diagnosed as diabetes when they consult their doctor for some other health reason.
Alterations in glucose metabolism by skeletal muscle and liver, the key insulin-responsive organs that monitors normal glucose homeostasis are seen in Type 2 Diabetes condition (Lowell et al, 2005). Adiponectin, an insulin sensitizing hormone from adipocytes, is a key factor for predicting T2DM (Hara et al., 2005). Drug-related and idiopathic acanthosis nigricans or familial acanthosis nigricans have been reported. IGF-1 receptors are expressed on basal keratinocytes and are upregulated in proliferative conditions. In some cases, oral, esophageal, pharyngeal, laryngeal, conjunctival, and anogenital mucosal surfaces may be involved. Still now, we not fully understand the actual causes of this diabetes; however, scientists believe both genetic factors with environmental triggers may involve. In the initial stages, insulin resistance is compensated by the hyper-secretion of insulin by the pancreatic ? cells. The increased levels of non-esterified fatty acid (NEFA), glycerol, Tumor Necrosis Factor-? (TNF-?), and cytokines in the blood plasma lead to the increased level of insulin resistance and reduced insulin sensitivity (Steven et al., 2006).


In general, though, acanthosis nigricans should be considered a prognostic indicator for developing type 2 diabetes.
Studies show that high concentrations of insulin stimulate fibroblast proliferation through IGF-1 receptors in vitro. In general, however, the back of the neck is the most consistently and severely affected area.
Diet or lifestyle has no link with the cause of type 1 diabetes, thus you cannot get rid of it. As insulin resistance increases, the plasma glucose level increases due to the lower insulin sensitivity and the normal functionality of the pancreatic ? cells is lost, leading to hyperglycemia (Weir et al, 2004). In a large, population-based study from Galveston, Texas, acanthosis nigricans was present in 7 percent of school-age children. Other members of the tyrosine kinase receptor family, including the epidermal growth factor receptor and the fibroblast growth factor receptor, have been implicated in acanthosis nigricans. On binding to its receptor, insulin induces activation of the insulin-receptor kinase (IRK) through autophosphorylation. This percentage increased to 66 percent of children who weighed 200 percent of their ideal body weight. Several genetic syndromes [Crouzon and SADDAN (severe achondroplasia with developmental delay and acanthosis nigricans)] with mutations in fibroblast growth factor receptor 3 result in acanthosis nigricans in the absence of hyperinsulinemia or obesity. In particularly florid cases, involvement on the back of the hands over the knuckles and even on the palms can be seen.
In patients with acanthosis nigricans in association with malignancy, there is usually improvement following treatment of the underlying malignancy.
Recruitment of insulin-receptor substrate (IRS) proteins induces activation of phosphatidylinositol 3-kinase (PI3K) through binding the p85 subunit and activating the catalytic p110 subunit. In this study, fasting insulin levels correlated with the presence and severity of skin findings. PI3K activation induces downstream effectors, such as phosphatidylinositol-dependent kinase 1 (PDK1) and protein kinase B (PKB; also known as AKT), leading to translocation of glucose transporter 4 (GLUT4) and glucose uptake in muscle, and inactivation of glycogen-synthase kinase 3 (GSK3).
When it is associated with malignancy, a tumor of intra-abdominal origin, usually gastric, is seen in the majority of cases. IR activation can also activate the c-Cbl-associated protein (CAP) and mitogen-activated protein kinase (MAPK) pathways (not shown). In the Galveston study, despite similar obesity rates, the prevalence was lower in whites (0.5 percent) and Hispanics (5 percent) than in African American children (13 percent).
It has been repeatedly described that patients' skin improves with chemotherapy and remits with recurrences. This finding suggests a possible genetic predisposition or increased sensitivity of the skin to hyperinsulinemia among certain populations. Activation of STAT3 through JAK2 phosphorylation induces translocation of STAT3 to the nucleus. Although historical data have emphasized the relationship between acanthosis nigricans and malignancy, a true association is rare. STAT3 induces gene responses that reduce transcription of acetyl-coenzyme-A carboxylase (ACC), reducing malonyl CoA and fatty-acid synthesis, while increasing fatty-acid oxidation. Only when the onset is particularly rapid, the clinical findings are florid, or in the non-obese or non-diabetic adult with acanthosis nigricans is an evaluation for malignancy beyond routine age appropriate screening warranted .
Endoplasmic-reticulum-bound or cytosolic PTP1B dephosphorylates membrane-bound or endocytosed insulin receptors and leptin receptors, causing their deactivation. In one author's experience with seeing more than 12,000 patients with cancer, only two developed acanthosis nigricans.
Other PTP1B substrates, such as IRS1 and PTP1B, can downregulate IRK activity through a complex formed with growth-factor-receptor-bound protein 2 (GRB2).



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