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

We examined the effect of short- and long-term exercise on prostacyclin (prostaglandin I2 [PGI2]) and thromboxane A2 (TXA2) synthesis in type I (insulin-dependent) diabetic patients and healthy control subjects. PGI2 synthesis was assessed by determining the urinary excretion of 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha and TX synthesis by measuring TXB2 in serum and urine. In the resting state, prostanoid excretion and concentrations were similar in diabetic and control subjects. During 40 min of ergometric cycling exercise, the urinary excretion of 6-keto-PGF1 alpha (a hydration product of vasodilatory PGI2) increased 5.8-fold more in the 12 control subjects than in the 15 diabetic patients (P less than .02). Serum TXB2 concentration rose similarly in diabetic patients and control subjects (P less than .05). During a 75-km competitive cross-country ski race (7 h, 30 min), urinary excretion of 6-keto-PGF1 alpha rose 1.9-fold in 7 diabetic (P less than .05) and 3.3-fold in 10 control (P less than .001) subjects, whereas urinary dinor excretion, reflecting vascular PGI2 synthesis more closely, increased only in the control subjects (P less than .01). Urinary TXB2 excretion remained unchanged in both groups during long-term exercise. These data suggest that diabetic patients have normal PGI2 and TXA2 synthesis in the resting state but diminished PGI2 response to both acute and prolonged exercise.
Diabetes Care 1989 Oct
PMID:Stimulation of prostacyclin synthesis by physical exercise in type I diabetes. 250 64

Due to a well known experience physical work in patients with diabetes mellitus II is a very important part of the therapy beside diet and medicament treatment. To guarantee a high training efficiency an individual training regimen has to be worked out for the patient. To influence the impaired glucose metabolism the endurance exercise should be carried out at an intensity near the anaerobic threshold. Therefore it is necessary to have a stepwise incremental exercise test including lactate determination after each work load of the patient. Basing on exercise test this paper is designed to give an example of a training regimen in various sport activities (bicycle, running, ski cross country running, swimming) which enables the physician to handle his diabetic patient with an stepwise increasing training program to an optimal training intensity.
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PMID:[Principles and general practice of a goal-oriented training plan for diabetic patients participating in sports]. 321 60

In Japan, diabetic patients are known to be able to sit on the floor for a prolonged time because of mildness or absence of ischemic paresthesia. In order to investigate this resistance to ischemia quantitatively, the mixed nerve function of the median nerve was studied during 30 min of ischemia using surface electrodes in 60 diabetic patients and 15 normal subjects. In studies of 33 unequivocal diabetics, potential amplitudes decreased during ischemia more slowly than in the controls, and at 15 min of ischemia, potential amplitudes were greater in all 33 diabetics than in the 15 normal subjects. The relationship between the resistance to ischemia and various aspects of diabetes was studied further in the 60 diabetics including the 33 aforementioned patients. Resistance to ischemia was found in almost all diabetics and no significant correlation was shown with values for fasting blood glucose and HbA1c, other diabetic complications or duration of diabetes. However, values for potential amplitudes declined to the normal range in seven of 18 patients after strict glucose control. These results suggest that resistance to ischemia is the earliest manifestation of peripheral nerve dysfunction and is different from classical diabetic neuropathy. Furthermore, the method employed in this study is simple, noninvasive and clinically very useful.
Diabetes Res Clin Pract
PMID:Effect of ischemia on peripheral nerve function in diabetes mellitus. 378 Mar 80

The purposes of this study of patients referred for renal transplant were to describe muscle strength impairments and deficits in gait performance and to establish the relationship between them. Twenty-six patients were tested. Muscle strength measurements included grip, elbow flexion, and shoulder abduction in the upper extremities, and ankle dorsiflexion, knee extension, hip abduction, and timed sit-to-stands in the lower extremities. Gait performance (level ground and stair) was quantified using ordinal scales and speed. Compared with healthy control subjects, patients demonstrated impairments in muscle strength and deficits in gait performance. Patients with diabetes demonstrated greater impairments and deficits than patients without diabetes. Patients with an active fistula demonstrated better grip strength in their upper extremity without the fistula. Gait performance was correlated significantly with lower extremity strength, with knee extension strength and weight providing the best prediction of gait speed (R2 = 0.478 to 0.617). The results of this study suggest that patients referred for renal transplantation possess both strength impairments and deficits in gait performance, the latter being related to the former. The clinician wishing to efficiently monitor strength impairments among patients referred for transplantation can obtain a reasonable indication of them from dynamometric grip and knee extension strength measurements.
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PMID:Muscle strength impairments and gait performance deficits in kidney transplantation candidates. 807 73

A heart-perfusion technique was employed to measure 125I-insulin binding on capillary endothelial and myocyte cell membranes in Sprague-Dawley rats. Animals were anesthetized, and the anterior chest wall excised to expose the mediastinal contents. The right and left superior and inferior venae cavae were dissected and tied, and another tie was passed around the aorta. A polyethylene catheter was introduced into the aortic lumen from cephalad to caudad to sit with its tip above the aortic valve. Another catheter was introduced into the cavity of the right atrium and both were anchored by sutures. Oxygenated Ringer-Lock buffer containing 20 mM/L K+ and 125I-insulin was perfused at a rate of 1 mL/min via the aortic catheter. Concomitantly, the distal ascending aorta and venae cavae were ligated. The effluent was collected from the right atrial catheter at the same infusion rate. Animals were divided into two groups, the normal group and streptozotocin-induced diabetic group. Heart perfusion was done on both groups either without or after treatment with detergent (CHAPS) to remove the capillary endothelial lining. A physical model for 125I-insulin sequestration as a ligand to its receptors on endothelial and/or myocyte plasma membranes was proposed. The model described a reversible binding of ligand on cellular surface receptor concentration to fit a conservation equation and a first order Bessel function. The binding constants (kn), reversal constants (k-n), dissociation constants kd = k-n/kn, and residency time constants tau = 1/k-n of 125I-insulin in normal untreated, normal CHAPS-treated, diabetic untreated, and diabetic CHAPS-treated hearts were estimated using a theoretically generated curve-fit to the data. Since insulin receptor binding on the capillary endothelial cell surfaces may serve to transport insulin from the intravascular to the subendothelial space, and since streptozotocin-induced diabetes was shown to diminish receptor autophosphorylation and kinase activity and hence internalization of insulin, then one can conclude the following from the data. In the normal heart, removal of the capillary endothelial lining with CHAPS did not alter kn, k-n, kd, and tau of insulin binding as compared to the normal untreated, whereas in the diabetic untreated heart these constants were altered, compared to the diabetic treated. Furthermore, the kn and k-n values in the diabetic CHAPS-treated hearts were the same as for the normals untreated and CHAPS-treated, respectively. In conclusion, the dissociation constants and residency time constants of all groups indicated the possible existence of two types of insulin receptors: the capillary endothelial cell surface insulin receptors with lower residency time (low affinity receptor or combination of insulin and IGF-1 receptors) and the myocyte plasma membrane insulin receptors with higher residency times (high affinity).
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PMID:Binding of 125I-insulin on capillary endothelial and myofiber cell membranes in normal and streptozotocin-induced diabetic perfused rat hearts. 921 56

Many consider diabetic autonomic neuropathy to be an irreversible complication of diabetes of long duration. Three patients developed symptoms of autonomic neuropathy which subsequently resolved. Their autonomic neuropathy was not associated with long duration of diabetes, but with weight loss. Each had marked weight loss and resolution occurred on regaining remembered premorbid weight. A woman aged 20 was admitted with anorexia nervosa (weight loss 6 kg). She complained of feeling bloated. Gastroenterological investigations showed delayed gastric emptying. RR ratio (respiration and standing) was abnormal. Resolution occurred after two years. A male aged 18 developed diabetic symptoms, which were overlooked. Twelve months later he presented underweight and ketonuric; insulin treatment was started but within one month he became impotent. Resolution occurred after 18 months. An 80 year old man presented after six months trial of diet and sulphonylurea therapy. He was underweight, had ketonuria, and such muscle loss that he was unable to sit unaided. Insulin treatment was started. He developed severe symptomatic postural hypotension. This resolved six months later by which time he had regained his normal weight. These cases illustrated symptomatic autonomic neuropathy occurring in relation to weight loss with resolution on recovery of normal weight, a temporal pattern mimicking that of acute cachectic painful neuropathy. Treatment of autonomic neuropathy should be like that of cachectic neuropathy, that is with an expectation of recovery and should include strategies to regain premorbid weight and achieve glycaemic control.
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PMID:Resolution of diabetic autonomic neuropathy. 1215 92

Type 1 diabetes is a systemic autoimmune disease that can be cured by transplantation of hematopoietic stem cells (HSCs) from disease-resistant donors. Nonobese diabetic (NOD) mice have a number of features that distinguish them as bone marrow transplant recipients that must be understood prior to the clinical application of chimerism to induce tolerance. In the present studies, we characterized NOD HSCs, comparing their engraftment characteristics to HSCs from disease-resistant strains. Strikingly, NOD HSCs are significantly enhanced in engraftment potential compared with HSCs from disease-resistant donors. Unlike HSCs from disease-resistant strains, they do not require graft-facilitating cells to engraft in allogeneic recipients. Additionally, they exhibit a competitive advantage when coadministered with increasing numbers of syngeneic HSCs, produce significantly more spleen colony-forming units (CFU-Ss) in vivo in allogeneic recipients, and more granulocyte macrophage-colony-forming units (CFU-GMs) in vitro compared with HSCs from disease-resistant controls. NOD HSCs also exhibit significantly enhanced chemotaxis to a stromal cell-derived factor 1 (SDF-1) gradient and adhere significantly better on primary stroma. This enhanced engraftment potential maps to the insulin-dependent diabetes locus 9 (Idd9) locus, and as such the tumor necrosis factor (TNF) receptor family as well as ski/sno genes may be involved in the mechanism underlying the autonomy of NOD HSCs. These findings may have important implications to understand the evolution of autoimmune disease and impact on potential strategies for cure.
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PMID:Hematopoietic stem cells from NOD mice exhibit autonomous behavior and a competitive advantage in allogeneic recipients. 1552 53

It is not uncommon for people to spend one-half of their waking day sitting, with relatively idle muscles. The other half of the day includes the often large volume of nonexercise physical activity. Given the increasing pace of technological change in domestic, community, and workplace environments, modern humans may still not have reached the historical pinnacle of physical inactivity, even in cohorts where people already do not perform exercise. Our purpose here is to examine the role of sedentary behaviors, especially sitting, on mortality, cardiovascular disease, type 2 diabetes, metabolic syndrome risk factors, and obesity. Recent observational epidemiological studies strongly suggest that daily sitting time or low nonexercise activity levels may have a significant direct relationship with each of these medical concerns. There is now a need for studies to differentiate between the potentially unique molecular, physiologic, and clinical effects of too much sitting (inactivity physiology) separate from the responses caused by structured exercise (exercise physiology). In theory, this may be in part because nonexercise activity thermogenesis is generally a much greater component of total energy expenditure than exercise or because any type of brief, yet frequent, muscular contraction throughout the day may be necessary to short-circuit unhealthy molecular signals causing metabolic diseases. One of the first series of controlled laboratory studies providing translational evidence for a molecular reason to maintain high levels of daily low-intensity and intermittent activity came from examinations of the cellular regulation of skeletal muscle lipoprotein lipase (LPL) (a protein important for controlling plasma triglyceride catabolism, HDL cholesterol, and other metabolic risk factors). Experimentally reducing normal spontaneous standing and ambulatory time had a much greater effect on LPL regulation than adding vigorous exercise training on top of the normal level of nonexercise activity. Those studies also found that inactivity initiated unique cellular processes that were qualitatively different from the exercise responses. In summary, there is an emergence of inactivity physiology studies. These are beginning to raise a new concern with potentially major clinical and public health significance: the average nonexercising person may become even more metabolically unfit in the coming years if they sit too much, thereby limiting the normally high volume of intermittent nonexercise physical activity in everyday life. Thus, if the inactivity physiology paradigm is proven to be true, the dire concern for the future may rest with growing numbers of people unaware of the potential insidious dangers of sitting too much and who are not taking advantage of the benefits of maintaining nonexercise activity throughout much of the day.
Diabetes 2007 Nov
PMID:Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease. 1782 99

This study investigated the use of electronic, web-enabled touch-screen information kiosks as a tool to provide culturally and linguistically appropriate diabetes information to Latino audiences. Two kiosk models (high privacy sit-down, group enabled stand-up) in two locations (pharmacy, community center) in Northeast Georgia provided bilingual, read-aloud diabetes education and local resource information on health care. Data from public use and interviews with focus group participants showed that users found the kiosks and their functions helpful and usable, though usage was moderated by presence or absence of a peer health educator (promotora); participants also preferred the sit-down, multi-function kiosk model.
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PMID:Disseminating health information and diabetes care for Latinos via electronic information kiosks. 1839 35

Friedreich ataxia (FRDA) is a rare autosomal recessive hereditary disorder that affects approximately 1 in 50,000 Caucasians. It is caused by hyperexpansion of GAA repeats in the first intron of the frataxin gene. Initial symptoms of FRDA usually appear around the beginning of the second decade of life. In addition to neuropathological disabilities such as ataxia, sensory loss, and muscle weakness, common signs are scoliosis, foot deformity, and hypertrophic cardiomyopathy. Approximately 10 % of patients with FRDA develop diabetes. The neuronopathy in the dorsal root ganglia, accompanied by the loss of peripheral sensory nerve fibres and the degeneration of posterior columns of the spinal cord, is a hallmark of the disease and is responsible for the typical combination of signs and symptoms specific to FRDA. Variation in neurophysiological abnormalities is correlated with the size of the GAA repeat expansion and likely accounts for individual variation in the progression of FRDA. Despite a range of disease severity, most patients will lose their ability to walk, stand, or sit without support within 10 to 15 years of disease onset. In addition to a review of the clinicopathological features of FRDA, a discussion of recent advances in our understanding of the underlying molecular mechanisms is provided.
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PMID:Friedreich ataxia: the clinical picture. 1928 44


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