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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a rare case of hypothermia with acute renal failure in a patient suffering from diabetic nephropathy. A 71-year-old male who had been receiving insulin therapy for the treatment of diabetes mellitus complicated with advanced diabetic nephropathy since 1998 was malnourished with an extremely decreased muscle mass. Without any prolonged exposure to excessively low external temperatures or hypothyroidism, pituitary insufficiency, adrenal insufficiency, sepsis, hypoglycemia, and diabetic ketoacidosis, acute hypothermia appeared together with an aggravation of diabetic nephropathy. His skin temperature fell to below measurable levels and his rectal temperature fell to 30.0 degrees C. His consciousness was drowsy and the hypothermia was not accompanied by shivering. Skeletal muscle is known to play an important role as a center of heat production and shivering thermogenesis in skeletal muscle mainly operates on acute cold stress. Therefore, in this case, hypothermia may have occurred because the shivering thermogenesis could not fully act on the acute cold stress due to the dramatically reduced muscle mass. We should always keep in mind that older, malnourished diabetic patients can easily suffer from impairments of the thermoregulatory system.
Diabetes Metab 2000 Apr
PMID:Hypothermia with acute renal failure in a patient suffering from diabetic nephropathy and malnutrition. 1080 30

When faced by an external aggression such as shock, sepsis, burns or surgery, the body develops a response, known as stress, comprising hypermetabolism and hypercatabolism related to an alteration in tissue sensitivity to insulin. This alteration seems to be rooted in the transmembrane protein GLUT-4 which takes care of the cell uptake of glucose in skeletal muscle. As a result, there are alterations in the metabolism of carbohydrates, fats and proteins (reduction of immunoglobulins). In the case of surgery, it has been shown that, on the one hand, factors such as rest, pre-operative fasting or the release of inflammatory response factors constrain an even greater alteration in the sensitivity to insulin; and on the other hand that the degree of resistance to insulin depends on the magnitude of the surgery, its duration, bleeding, or on hypothermia and extracorporeal circulation in the case of heart surgery. These metabolic alterations may lead to an increase in the number of infections, mean stay in hospital, and even lead to diabetes mellitus in the long term. Over the last few years, all of this has led several researchers to try to minimize the stress response associated with planned surgery through replacing pre-operative fasting by the administration of carbohydrates, whether or not in association with insulin in perfusion. Beneficial results have been described: control of hyperglycaemia, lower consumption of neoglycogenic amino acids and less alteration of plasma immunity (interleukins, TNF). Future studies will evaluate the influence of these measures on plasma immunity, mean hospital stay and morbidity/mortality.
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PMID:[Metabolic response to stress, can we control it?]. 1121 95

Brain dopaminergic pathways play a major role in the control of movement. Absence of the murine dopamine D2 receptor gene (drd2) produces bradykinesia and hypothermia. A Ser311Cys mutation of the human DRD2 produces a marked functional impairment of the receptor and is associated with higher BMI in some populations. We hypothesized that the Ser311Cys mutation of DRD2 may inhibit energy expenditure. Here we report that total energy expenditure (doubly labeled water) measured in 89 nondiabetic Pima Indians was 244 kcal/ day lower in homozygotes for the Cys311-encoding allele when compared with those heterozygous and homozygous for the Ser311-encoding allele (P = 0.056). The 24-h resting energy expenditure (respiratory chamber) measured in 320 nondiabetic Pimas was also 87 kcal/day lower in homozygotes for the Cys311-encoding allele when compared with those heterozygous and homozygous for the Ser311-encoding allele (P = 0.026). These findings are the first evidence that a genetic mutation is associated with reduced energy expenditure in humans. Because the impact of this mutation on human obesity is small, we suggest that either the energy deficit induced is not large enough to significantly influence body weight in this population and/or that the Cys311-encoding allele is also associated with reduced energy intake.
Diabetes 2001 Apr
PMID:A Ser311Cys mutation in the human dopamine receptor D2 gene is associated with reduced energy expenditure. 1128 60

Although the incidence of overt sequelae has traditionally been higher in patients undergoing isolated intracardiac procedures such as valve replacement or repair, recent studies show that the incidence of stroke for intracardiac procedures now approximates that for isolated coronary artery bypass grafting (CABG), in the range of 1 to 4%. In both intracardiac and extracardiac surgery, macroemboli (>200 microm in diameter) and microemboli (<40 microm in diameter) seem to be responsible for most neurologic complications. The risk of overt stroke is clearly increased in patients who undergo more complicated, combined procedures such as CABG plus valve replacement or CABG plus carotid endarterectomy. For isolated CABG, preoperative risk factors include advanced patient age, proximal aortic atherosclerosis, hypertension, previous stroke or transient ischemic attack, diabetes, and female gender. One area of controversy and current research concerns whether hypothermia is better than normothermia during cardiopulmonary bypass (CPB). Another debatable issue is whether CPB itself results in neurologic damage, owing to nonpulsatile perfusion, complement activation and the "inflammatory response," or a greater propensity for platelet activation and aggregation into microemboli in this setting. Strategies for preventing adverse neurologic outcome (new paradigms for managing intra-aortic plaque and controlling the cerebral reperfusion temperature) and for acute intervention (using specific cerebral protective agents) are under investigation. Further research into techniques for preventing or mitigating cerebral injury, particularly in high-risk patients, is clearly mandated.
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PMID:A review of risk factors for adverse neurologic outcome after cardiac surgery. 1191 28

Professional phagocytes, comprising polymorphonuclear neutrophils and monocyte/macrophage cells, play an important role in the host defense. Any defect in their function exposes the organism to microbial intruders terminating in fatal diseases. The functional responses of the phagocytes to bacterial and fungal infections include chemotaxis, actin assembly, migration, adhesion, aggregation, phagocytosis, degranulation, and reactive oxygen species production. Superoxide generation by phagocytic NADPH oxidase is an imperative step toward bacterial killing. Phagocytes participate in inflammatory reactions and exert tumoricidal activity. They are supported by serum factors such as immunoglobulins, cytokines, complement, the acute phase reactant C-reactive protein, production of antibacterial proteins, and others. In addition to their principal task to eliminate bacteria, they are engaged in removing damaged, senescent, and apoptotic cells. Engulfed cell debris, large particles such as latex beads, fat, and oil droplets, are examples of phagocytic activity illustrated in the present review with transmission and scanning electron microscope micrographs. Numerous factors, such as diseases and stressful conditions, affect the engulfing activity of the professional phagocytes. Our experience regarding the impaired phagocytic capacity of cells in patients with diabetes and chronic renal failure is discussed. The results obtained in our laboratory from experiments detecting the effect of strenuous physical exercise, hypothermia, fasting, and abdominal photon irradiation on the phagocytic capacity of human polymorphonuclear neutrophils and rat peritoneal macrophages are hereby summarized and the reports on those subjects in the recent literature are reviewed. A variety of assays are applied for quantifying phagocytosis. Flow cytometry based on incubation of phagocytic cells with fluorescent conjugated particles and measuring the amount of fluorescence as an indicator of the engulfing capacity of the cells is a useful method. A direct visualization of the ingested particles using light or electron microscopy is a valuable tool for estimation of phagocytic function. In our hands, the use of semithin sections of embedded phagocytes following their incubation with latex particles provided satisfactory results for measuring the total number of phagocytic cells, as well as the internalizing capacity of each individual cell. Microbiological assays, the nitroblue tetrazolium test, quantitation of antibody- and antigen-mediated phagocytosis, as well as methods reviewed in detail in other reports are additional applications for determination of this intricate process.
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PMID:Phagocytosis--the mighty weapon of the silent warriors. 1211 25

Leptin contributes to the regulation of thermogenesis. In rodents, sympathetic nerve activity efferent to interscapular brown adipose tissue (IBAT-SNA) is involved. On the basis of the hypotheses that 1) leptin acutely potentiates hypothermia-induced increases in IBAT-SNA; 2) this action of leptin is specific to IBAT-SNA, i.e., it does not occur with renal sympathetic nerve activity (R-SNA); and 3) this effect of leptin depends on intact and functional leptin receptors, we measured IBAT-SNA and R-SNA in anesthetized lean and diet-induced obese Sprague-Dawley and in obese Zucker rats, randomly assigned to low-dose leptin or vehicle. Before the start of leptin or vehicle and 5 min, 90 min, and 180 min after, hypothermia (30 degrees C) was induced. Compared with vehicle, leptin did not significantly alter baseline R-SNA or IBAT-SNA. In lean Sprague-Dawley rats, hypothermia-induced increases in IBAT-SNA were significantly augmented by leptin but not by vehicle. In obese Sprague-Dawley rats, leptin did not potentiate hypothermia-induced increases in IBAT-SNA. In Zucker rats, IBAT-SNA did not increase with hypothermia and leptin was not able to induce sympathoactivation with cooling. Changes in R-SNA during hypothermia were not significantly modified by leptin in either group. Thus, low-dose leptin, although not altering baseline SNA, acutely enhances hypothermia-induced sympathetic outflow to IBAT in lean rats. This effect is specific for thermogenic SNA because leptin does not significantly alter the response of R-SNA to hypothermia. The effect depends on intact and functional leptin receptors because it occurs neither in rats with a leptin receptor defect nor in rats with acquired leptin resistance.
Diabetes 2002 Aug
PMID:Leptin potentiates thermogenic sympathetic responses to hypothermia: a receptor-mediated effect. 1214 55

Lower limb compartment syndrome is an unusual but severe complication of prolonged surgery more than four hours in lithotomy position. It is usually a consequence of hypoperfusion of the lower extremities and muscle necrosis may occur. Several risk factors are pointed out: trendelenburg, the hardness of operating table, hypothermia, control hypotension, occlusion of arterial blood flow of the lower extremity, arteritis (and smoking), diabetes, obesity, arterial hypertension, myopathy and an important muscle mass. The symptoms are postoperative pain with neurological signs. A rapid diagnosis and aggressive management (i.e. resuscitation and aponevrotomy) is recommended. Neurological sequelae are sometimes invalidating. Reporting a case of bilateral syndrome, we reviewed the literature and describe the present diagnosis and therapeutic management as well as prevention modalities of this iatrogenic complication.
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PMID:[Bilateral compartment syndrome after colorectal surgery in the lithotomy position]. 1240 49

Hypothalamic proopiomelanocortin (POMC) gene expression is reduced in many forms of obesity and diabetes, particularly in those attributable to deficiencies in leptin or its receptor. To assess the functional significance of POMC in mediating metabolic phenotypes associated with leptin deficiency, leptin-deficient mice bearing a transgene expressing the POMC gene under control of the neuron-specific enolase promoter were produced. The POMC transgene attenuated fasting-induced hyperphagia in wild-type mice. Furthermore, the POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized hyperglycemia, glucosuria, glucose intolerance, and insulin resistance in leptin-deficient mice. Effects of the POMC transgene on glucose homeostasis were independent of the partial correction of hyperphagia and obesity. Furthermore, the POMC transgene normalized the profile of hepatic and adipose gene expression associated with gluconeogenesis, glucose output, and insulin sensitivity. These results indicate that central POMC is a key modulator of glucose homeostasis and that agonists of POMC products may provide effective therapy in treating impairments in glucose homeostasis when hypothalamic POMC expression is reduced, as occurs with leptin deficiency, hypothalamic damage, and aging.
Diabetes 2003 Nov
PMID:Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice. 1457 85

Neonatal diabetes mellitus (NDM) is a very rare disease defined as hyperglycemia that occurs during the first month of life, requires insulin treatment, and lasts more than 2 weeks. There are 2 types of NDM: permanent neonatal diabetes mellitus (PNDM) and transient neonatal diabetes mellitus (TNDM). We report a case of PNDM in a 3-day-old female infant. This full-term neonate was born small for gestational age. Respiratory distress, poor activity, hypothermia, poor feeding, dehydration, and ketoacidosis were noted at the age of 3 days. After insulin therapy and fluid replacement, her condition became stable. Glucagon test done at the age of 26 days showed serum C-peptide level to be low for her age. During the first year of life she had catch-up growth, but insulin therapy was still required. Serum C-peptide level was undetectable at the age of 15 months. The course of this case indicates the importance of a high index of suspicion for patients with PNDM in order to correct metabolic derangement as early as possible and facilitate normal growth and development under insulin therapy.
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PMID:Permanent neonatal diabetes mellitus manifesting as diabetic ketoacidosis. 1497 69

The Dio2 gene encodes the type 2 deiodinase (D2) that activates thyroxine (T4) to 3,3',5-triiodothyronine (T3), the disruption of which (Dio2(-/-)) results in brown adipose tissue (BAT)-specific hypothyroidism in an otherwise euthyroid animal. In the present studies, cold exposure increased Dio2(-/-) BAT sympathetic stimulation approximately 10-fold (normal approximately 4-fold); as a result, lipolysis, as well as the mRNA levels of uncoupling protein 1, guanosine monophosphate reductase, and peroxisome proliferator-activated receptor gamma coactivator 1, increased well above the levels detected in the cold-exposed wild-type animals. The sustained Dio2(-/-) BAT adrenergic hyperresponse suppressed the three- to fourfold stimulation of BAT lipogenesis normally seen after 24-48 h in the cold. Pharmacological suppression of lipogenesis with betabeta'-methyl-substituted alpha-omega-dicarboxylic acids of C14-C18 in wild-type animals also impaired adaptive thermogenesis in the BAT. These data constitute the first evidence that reduced adrenergic responsiveness does not limit cold-induced adaptive thermogenesis. Instead, the resulting compensatory hyperadrenergic stimulation prevents the otherwise normal stimulation in BAT lipogenesis during cold exposure, rapidly exhausting the availability of fatty acids. The latter is the preponderant determinant of the impaired adaptive thermogenesis and hypothermia in cold-exposed Dio2(-/-) mice.
Diabetes 2004 Mar
PMID:Mice with targeted disruption of the Dio2 gene have cold-induced overexpression of the uncoupling protein 1 gene but fail to increase brown adipose tissue lipogenesis and adaptive thermogenesis. 1498 40


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