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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overload of the beta cell, mediated by a variety of mechanisms, may sensitise it to immune damage and apoptosis, and thus accelerate ongoing autoimmune processes leading to its destruction. Environmental risk determinants that may exert such overload effects include insulin resistance due to excess fat cell accumulation, and increased insulin requirement due to a high growth rate, physical stress (infection, inflammation) or psychological stress. The increasing incidence of childhood diabetes, and the shift to younger age at onset, is unlikely to be driven by environmental risk factors that have been associated with initiation of autoimmunity, e.g. virus infections or early infant feeding. Risk factors that may accelerate beta cell destruction have shown a steady increase in the population, and are more plausible causes of such a pattern of change. Child growth, weight and birthweight are well-established estimates of community wealth and increase in most countries of Europe. Overfeeding of children early in life leads to both accelerated growth and weight, and even a moderate excess of child growth, not necessarily associated with obesity, is associated with risk of type 1 diabetes. New, safe and effective immune-modulating drugs for possible arrest of the autoimmune process may become available in time, but in the interim these accelerating factors may be targeted. Public health programmes for pregnant mothers and young families, aiming at changing overfeeding and the sedentary lifestyle of the children would be preferable to other alternatives. Interventions such as these would be safe and could potentially influence future risks of type 1 and type 2 diabetes and other major threats to adult health.
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PMID:Can we slow the rising incidence of childhood-onset autoimmune diabetes? The overload hypothesis. 1636 79

Repeated mental stress may lead to chronic alterations in cortisol and catecholamine concentrations and to insulin resistance. Furthermore, chronically elevated cortisol concentrations may favour the development of abdominal obesity and of the metabolic syndrome. Oxidative stress impairs glucose uptake in muscle and fat and correlates with BMI. Obese subjects with type 2 diabetes, especially soon after the onset of diabetes, usually exhibit postprandial hyperglycemia with delayed hyperinsulinemia. It is recognized that insulin resistance causes postprandial hyperglycemia; however, it is also possible that impairment of early insulin secretion in response to an oral glucose load is the reason why postprandial hyperglycemia occurs. Since even modest increases in postprandial glucose values can be a risk factor for cardiovascular disease. Therefore, the effects of palatinose based functional food which reduces postprandial hyperglycemia and hyperinsulinemia were investigated in rats. This novel food definitely reduced visceral fat accumulation and improved insulin sensitivity. Therefore, it is suggested that functional food which suppresses postprandial glucose level is beneficial for both stress and metabolic controls.
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PMID:Control of oxidative stress and metabolic homeostasis by the suppression of postprandial hyperglycemia. 1636 12

Psychological stress has been implicated as a cause of several psychosomatic disorders, but also as a factor that can unfavourably influence many diseases including diabetes mellitus. Measure of psychological stress in diabetes was performed by Psychological Stress Measure (PSM), a validated instrument, designed using 49 items drawn from descriptors generated by focus groups on stress. Clinical and psychological framework was assessed in a cohort of 100 type 2 diabetic patients (30 m, 70 f), aged 66.99 +/- 13.68 years considering disease grade, complications and level of instruction. Three other questionnaires were administered concurrently to all patients: Sickness Impact Profile (SIP), Functional Living Index (FLI) and SF-36 QOL. ANOVA statistical testing and Spearman correlation matrix were used also vs socio-cultural and clinical profile. Gender, obesity, diet compliance, smoking do not affect PSM response. Hypertensive patients and those with family history of diabetes show lower PSM scores, according to a sort of moderator effect on stress of concurrent and/or previous experience with chronic disease. Neuromuscular ailments are more prevalent in women; men vs women experience severe limitations of their working capacities and relational possibilities, with severe discomfort. In the whole, higher scores of PSM (greater stress p < 0.01) and lower scores of FLI (fair well-being perception; p < 0.01) are reciprocally related inside any school instruction level. Despite the great reciprocal association of the PSM vs FLI and SIP, no significant correlation is found between PSM vs SF-36 QOL. Socio-cultural elements interfere, and particularly instruction level quantified as school grades achieved, with the manner of living their disease. Interventions on psychological distress of type 2 diabetes mellitus patients is warranted, specially in the groups with lower levels of instruction which may need an attentive strategy for achieving a satisfactory coping with this disease.
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PMID:Psychological stress measure in type 2 diabetes. 1670 51

The communication between the central nervous system and the immune system occurs via a complex network of bidirectional signals linking the nervous, endocrine and immune systems. The field of psychoneuroimmunology (PNI) has provided new insights to help understand the pathophysiological processes that are linked to the immune system. Work in this field has established that psychological stress disrupts the functional interaction between the nervous and immune systems. Stress-induced immune dysregulation has been shown to be significant enough to result in health consequences, including reducing the immune response to vaccines, slowing wound healing, reactivating latent herpesviruses, such as Epstein-Barr virus (EBV), and enhancing the risk for more severe infectious disease. Chronic stress/depression can increase the peripheral production of proinflammatory cytokines, such as interleukin (IL)-6. High serum levels of IL-6 have been linked to risks for several conditions, such as cardiovascular disease, type 2 diabetes, mental health complications, and some cancers. This overview will discuss the evidence that psychological stress promotes immune dysfunction that negatively impacts human health.
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PMID:Stress-induced immune dysregulation: implications for wound healing, infectious disease and cancer. 1804 Aug 14

Obesity and type 2 diabetes continue to be major public health burdens with type 2 diabetes rising in epidemic proportions. Since known risk factors do not explain all of the variance in the population, it is important to identify novel risk factors that can lead to development of new preventive measures. Chronic psychological stress and depression are associated with type 2 diabetes but the mechanism remains unclear. Neuroendocrine changes induced by these stressors, specifically activation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS), might provide a unifying explanation. The objectives of this review are (1) to summarize the metabolic impact of HPA axis and SNS dysfunction induced by depression and stress, (2) to summarize the relation of neuroendocrine parameters to risk factors for diabetes, (3) to discuss the limitations of assessing neuroendocrine function in population-based and intervention studies, and (4) to summarize the evidence of the impact of stress reduction, by cognitive behavior therapy (CBT), on neuroendocrine factors and on outcomes in diabetes and obesity.
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PMID:A review of the evidence for a neuroendocrine link between stress, depression and diabetes mellitus. 1822 Jun 83

Obesity, lipid disorders, type 2 diabetes, high blood pressure and coronary heart disease are frequently encountered in wealthy populations. All these disorders frequently occur as clusters, constituting the metabolic syndrome. It is currently admitted that insulin resistance plays a central role in the pathogenesis of this syndrome. Stress responses include activation of the sympathetic nervous system and stimulation of epinephrine and cortisol release. These hormones may over the long term reduce insulin sensitivity. Cortisol may also favour the development of central obesity. In healthy individuals, mental stress increases heart rate, but simultaneously decreases vascular resistance in skeletal muscle. This results in a moderate increase in blood pressure, and an acute increase in insulin-mediated glucose disposal. In obese patients, mental stress elicits responses which differ widely from those of healthy individuals. While mental stress enhances catecholamine-mediated energy expenditure in obese patients to the same extent as in lean subjects, it fails to decrease systemic vascular resistance due to endothelial dysfunction. This leads to enhanced blood pressure responses and the absence of stimulation of glucose disposal in obese subjects during mental stress. It can be hypothesized that repeated professional or social stress may activate the sympathoadrenal system, resulting in high cortisol levels, stimulation of the sympathetic nervous system, and epinephrine secretion. All these factors may eventually lead to the development of central obesity and insulin resistance. Furthermore, the blood pressure responses to mental stress may be enhanced in insulin-resistant individuals, favouring the development of vascular complications.
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PMID:Stress and metabolism. 1837 Jul 4

The high prevalence of diabetes in African-American (AA) women has been widely assumed to be related to the greater prevalence of obesity in this group. Catecholamine release acting on central adipose tissue has been proposed to be a contributing factor. The aim of this article was to examine the interaction of plasma catecholamines and central adiposity on fasting and nonfasting glucose levels in two separate samples. In both studies, the women were healthy, nondiabetic of similar age. In addition, both studies assessed plasma epinephrine (EPI) and norepinephrine (NOREPI) levels collected at three time points. In study 1, catecholamines were measured during a standardized laboratory mental stress task and in study 2, they were measured during the initial phase (10 min) of an intravenous glucose tolerance test (IVGTT). Results from both studies revealed significant effects of EPI on fasting glucose in the obese women. In study 1, mean EPI levels were significantly related to fasting glucose in AA women with high trunk fat (beta = 0.60, P < 0.001). Because high BMI was associated with high trunk fat in women, we used BMI >30 as a proxy for high trunk fat (>32%) in study 2. In study 2, EPI response to the glucose bolus was a strong predictor of fasting glucose in AA women with BMI >30 (beta = 0.75, P < 0.003). We conclude that the effect of central adiposity on fasting glucose may be moderated by plasma EPI. This suggests that adrenal medullary activity could play a role in the pathophysiology of type 2 diabetes.
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PMID:Plasma epinephrine predicts fasting glucose in centrally obese African-American women. 2030 86

The current synthesis of the 'hygiene hypothesis' suggests that the recent increase in chronic inflammatory disorders is at least partly attributable to immunodysregulation resulting from lack of exposure to microorganisms that have evolved an essential role in the establishment of the immune system. This document provides a background for discussion of the following propositions. 1. The essential role of these organisms is an example of 'evolved dependence'. 2. The most relevant organisms are those that co-evolved with mammals, and already accompanied early hominids in the Paleolithic. 3. More recently evolved 'childhood infections' are not likely to have evolved this role, and recent epidemiology supports this contention. 4. This mechanism is interacting with other modern environmental changes that also lead to enhanced inflammatory responses [inappropriate diet, obesity, psychological stress, vitamin D deficiency, pollution (dioxins), etc.]. 5. The range of chronic inflammatory disorders that is affected is potentially larger than usually assumed [allergies, autoimmunity, inflammatory bowel disease, but also vascular disease, some cancers, depression/anxiety (when accompanied by raised inflammatory cytokines), and perhaps neurodegenerative disorders and type 2 diabetes].
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PMID:99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: darwinian medicine and the 'hygiene' or 'old friends' hypothesis. 2041 54

During acute psychological stress, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system are activated. The released stress hormones influence glucose metabolism, can activate immune cells, and modulate subclinical inflammation. The aim of our study was to analyze the effect of acute psychological stress on glucose metabolism and the inflammatory status in patients with post-traumatic stress disorder (PTSD). We included 15 overweight male Bosnian war refugees with PTSD into the study (mean age 44+/-11 years, BMI 29.3+/-4.3 kg/m (2)). All subjects underwent an oral glucose tolerance test (OGTT) with either acute stress (trauma script exposure) or a resting period in a cross-over design. Blood was drawn over 2.5 h and metabolic markers were measured. Systemic levels of immune markers were determined using high-sensitive ELISA or bead-based multiplex assay. Immune gene expression was quantified by RT-PCR. After being exposed to acute stress, cortisol levels and heart frequency tended to be increased. Higher blood glucose and insulin levels after stress exposure were observed (p<0.05). Systemic levels of the chemokines interferon-gamma-inducible protein-10 and macrophage chemoattractant protein-1 were decreased compared to the control day (both p<0.05) and the expression of the proinflammatory regulator IKK beta was significantly reduced after stress exposure (p<0.001). In conclusion, acute stress induces postprandial blood glucose peaks and elevated insulin levels and a selective decrease of systemic immune markers and the proinflammatory regulator of the NF kappaB cascade, which are associated with type 2 diabetes. This points towards an independent effect of acute psychological stress on glucose metabolism and inflammation.
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PMID:Effects of acute psychological stress on glucose metabolism and subclinical inflammation in patients with post-traumatic stress disorder. 2066 27

Previous research supports a relationship between psychological stress and chronic disease in Puerto Rican adults living in the Boston, Massachusetts area. Stress may affect health by influencing dietary and physical activity patterns. Therefore, perceived stress and two hypothesized mediators of stress-related food intake, insulin and cortisol, were examined for possible associations with dietary and activity patterns in >1300 Puerto Ricans (aged 45-75 years; 70% women) living in the Boston, Massachusetts area. Data were analyzed using multiple linear regression and ANCOVA. Greater perceived stress was associated with lower fruit, vegetable, and protein intake, greater consumption of salty snacks, and lower participation in physical activity. Stress was associated with higher intake of sweets, particularly in those with type 2 diabetes. Cortisol and stress were positively associated in those without diabetes. Cortisol was associated with higher intake of saturated fat and, in those with diabetes, sweet foods. Independent of diabetes, perceived stress was associated with higher circulating insulin and BMI. Our findings support a link between stress, cortisol, and dietary and activity patterns in this population. For high-sugar foods, this relationship may be particularly important in those with type 2 diabetes. Longitudinal research to determine causal pathways for these identified associations is warranted.
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PMID:Relationship between perceived stress and dietary and activity patterns in older adults participating in the Boston Puerto Rican Health Study. 2107 Aug 27


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