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

Increased microalbuminuria is seen early in rats with both streptozotocin-induced and genetic (Bio-Breeding) diabetes. This study examines the roles of angiotensin II-dependent mechanism(s) and sulfation of glomerular proteoglycans in this phenomenon, as both processes have been implicated by several lines of circumstantial evidence. Anionic sites in the glomerular basement membrane, attributed to the presence of heparan sulfate, were quantitated by polyethyleneimine staining at 15, 21, and 70 days of diabetes in rats treated with streptozotocin, with or without insulin, and at 70 days in the Bio-Breeding rats. All diabetic rats developed increased microalbuminuria: control, 0.08 +/- 0.03 microgram/mL glomerular filtration rate, mean +/- SD; streptozotocin without insulin at 15 days, 0.92 +/- 0.06 microgram/mL (p < 0.05); streptozotocin with insulin at 21 days, 0.61 +/- 0.37 microgram/mL (p < 0.05 vs. control). At 70 days, both the Bio-Breeding and the streptozotocin rats sustained their microalbuminuria to the same degree (p < 0.05 vs. control). Enalapril (250 mg/L) in the drinking water of diabetic animals did not reduce the microalbuminuria. Although the polyethyleneimine-stained heparan sulfate sites decreased significantly in the streptozotocin rats, they remained unchanged in the Bio-Breeding rats. To determine the cause of reduced heparan sulfate staining, the in vitro synthesis and degree of sulfation of proteoglycans by glomeruli isolated from control and streptozotocin diabetic rat kidneys were compared. The amount of heparan sulfate synthesis and degree of sulfation were unchanged in diabetic glomeruli, although lower incorporation into the extracellular matrix and greater secretion into the medium were noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased microalbuminuria in diabetic rats is independent of angiotensin II or glomerular proteoglycan synthesis. 147 41

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

The ability to quantify the yield of pancreatic islet tissue after isolation is important for interlaboratory comparisons and for the assessment of islet yield prior to clinical transplantation. Because pancreatic islets contain a much higher concentration of zinc than other tissues, we investigated the analysis of zinc as a measure of islet tissue yield. Rat islets of standard diameter 250 microns were handpicked into samples containing 10-80 islets. The zinc content was measured by EAAS and showed a linear correlation with islet number. A zinc binding fluorescent dye, TSQ, was investigated as a way of simplifying the zinc measurement for routine use. Samples of 10-80 islets of 250 microns were sonicated in 3 ml zinc-free water, 0.18 mumol TSQ was added, and the TSQ-zinc fluorescence was measured at 480 nm. A linear correlation was observed. Exocrine contamination up to 50% barely affected the results. Islet zinc content also was shown to be correlated linearly with islet number for freshly isolated human islets. Measurement of zinc by TSQ fluorescence is a rapid, cheap, and objective measure of islet tissue content.
Diabetes 1992 Sep
PMID:A new method for quantification of islets by measurement of zinc content. 149 58

In this study, total body fat content and fat topography were related to glucose metabolism in the basal and insulin-stimulated states in 18 nonobese and 18 obese premenopausal nondiabetic women. All subjects received a euglycemic insulin (20 mU.min-1.m2) clamp study in combination with [3-3H]-D-glucose infusion and indirect calorimetry to quantitate total body glucose uptake, glucose oxidation, and nonoxidative glucose disposal. Total body fat content was determined with tritiated water, whereas body fat distribution was estimated from the WHR, the STR, and the VSR (measured by magnetic resonance imaging). In the postabsorptive state, total body glucose utilization, glucose oxidation, and nonoxidative glucose disposal rates were similar in nonobese and obese women, whereas during the insulin clamp all three metabolic parameters were reduced significantly in the obese group. In nonobese women, total body fat content was related inversely to both total and nonoxidative glucose disposal during the insulin clamp, whereas no relationship was found between glucose metabolism (total, oxidative, and nonoxidative) and WHR, STR, or VSR. In contrast, in obese women, no relationship was observed between total body fat content and any measure of insulin-mediated glucose metabolism. However, both WHR and VSR were related inversely to total, oxidative, and nonoxidative glucose disposal rates during the insulin clamp. These results suggest that total body fat content and body fat topography are associated differently with insulin-mediated glucose metabolism in nonobese and obese women. In the nonobese women, total body fat mass appears to be a primary determinant of tissue sensitivity to insulin, whereas in obese women, body fat topography exerts a more dominant effect.
Diabetes 1992 Sep
PMID:Total body fat content and fat topography are associated differently with in vivo glucose metabolism in nonobese and obese nondiabetic women. 149 66

The interaction of the diabetes associated polypeptide (amylin) with dimyristoylphosphatidylcholine (DMPC) was assessed by measurements of turbidity (absorbance at 400 nm) and secondary structure by CD spectroscopy. In trifluoroethanol, human amylin adopts a highly alpha-helical conformation while the rat peptide is less structured. In water, the rat peptide is largely disordered and the human peptide exhibits a combination of alpha- and beta-structures. Mixtures of DMPC and the rat peptide have no effect on either the turbidity of the DMPC or the CD spectrum of the peptide. By contrast, mixtures of the human peptide with DMPC form relatively clear mixtures similar to those observed with amphipathic alpha-helical peptides, but the structure adopted, based on the CD spectrum, is largely beta. These data demonstrate that fundamental differences in the structures adopted by amylins from human and rat species exist in mixtures with DMPC and suggest that these differences may be related to the formation of amyloid fibrils in the human amylin peptide which are not observed in the rat peptide.
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PMID:Promotion of beta-structure by interaction of diabetes associated polypeptide (amylin) with phosphatidylcholine. 150 94

UNICEF promotes the use of a very effective, inexpensive treatment of dehydration in developing countries: oral rehydration therapy (ORT), which is oral administration of a solution with equimolar concentrations of sodium and glucose (osmolality of about 300 mosmol). The solution is isotonic with respect to total body water when it reaches the small intestine. It expands the extracellular fluid without changing serum osmolality, thus, brain edema does not occur. Further, metabolic degradation of glucose eventually releases free water. On the other hand, intravenous rehydration with saline solution can be lethal, causing excess free water to expand shrunken cells and, thereby, causing brain swelling, rupture of blood vessels and hemorrhage. Yet, physicians and other health workers in developed countries have been quite sow to accept ORT. Leading conditions of dehydration include insensible loss of water and heat through evaporation from the respiratory tract and skin (common in dry air, hot environment, and fever), sensible loss of water and heat through perspiration (common in hot, humid environment and with warm and absorbent clothing), and irritation of the intestinal mucosa by allergies, infections, toxins, and intolerance to some nutrients, resulting in diarrhea. Diarrhea is indeed the main cause of dehydration. Other causes of dehydration are: failure of the hypothalamus to secrete antidiuretic hormone (ADH), kidney unresponsiveness to ADH, diabetes mellitus, protein-rich nutrition, catabolic states, and brush-border lactase after weaning. Physiological changes in dehydration consist of rigidity of the connective tissue (vascular system and lungs) and intracellular fluid loss to the extracellular spaces, resulting in dry mucous membranes, shrunken muscle cells in the lips and the tongue, soft eyes, and adverse effects to the central nervous system. Children become dehydrated more readily than adults, but they tolerate it better.
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PMID:Water: mechanism of oral rehydration, water deficiency = deficiency in salt. 150 31

The concentration and distribution of labile elements in nerve cells is tightly regulated by multiple membrane transport processes and by binding to lipids and proteins. The multifaceted nature of elemental regulation provides numerous sites at which toxicants or disease processes might act to disrupt this regulation. Such disruption can affect cytoskeletal integrity, macromolecular synthesis, energy production, osmoregulation and other cellular processes. The possible role of perturbed elemental homeostasis in the mechanism of nerve injury caused by certain chemicals (e.g., acrylamide, 2,5-hexanedione) and neuropathic diseases (e.g., diabetes) has not been determined. To investigate this possibility, we have used electron probe x-ray micro-analysis (EPMA) to measure the distribution of elements and water in cellular compartments of myelinated axons (axoplasm, mitochondria) and glial cells (cytoplasm, myelin) in normal rat central and peripheral nervous systems. Results indicate that each compartment exhibits a characteristic composition of elements and water which might reflect function of that anatomical region or organelle. Injury-induced changes in elemental content of PNS axons and Schwann cells have been identified using several neurotoxic models (i.e., acrylamide, axotomy, diabetic neuropathy). Each type of injury initiated early alterations in element and water composition of both axons and glial cells. Compositional changes were specific and developed sequentially instead of simultaneously. Results of these studies suggest that, rather than being an epiphenomenon, altered elemental regulation might represent a primary component of many neurotoxic mechanisms.
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PMID:Perturbation of axonal elemental composition and water content: implication for neurotoxic mechanisms. 150 12

Vanadyl sulfate trihydrate was given by gavage to streptozotocin-induced diabetic rats for 21 days at doses of 0, 25, 50, or 75 mg/kg/day. In marked contrast to the reduction in plasma glucose observed in diabetic animals given vanadyl sulfate via drinking water, diabetic rats given vanadyl by gavage were not characterized by normoglycemia. Similarly, in contrast to the normalizing effect of vanadyl in drinking water, vanadyl by gavage had only a minimal influence on diabetes associated hyperphagia and polydipsia. Despite the lack of marked effect of vanadyl by gavage on the above parameters, tissue vanadium accumulation in the gavaged rats was similar to that reported for rats given vanadium by drinking water. The present results (taken together with previous data) show that the administration of vanadium by gavage is not a viable alternative to the use of insulin in diabetes treatment.
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PMID:Administration of vanadyl sulfate by gavage does not normalize blood glucose levels in streptozotocin-induced diabetic rats. 150 5

This study reports on the effect of streptozotocin (STZ) induced diabetes on water soluble-SH and -SS, as well as on hepatic glutathione peroxidase (GSH-Px), catalase and superoxide dismutase (SOD) activity and on malondialdehyde (MDA) content. In addition, we determined serum concentrations of glucose, cholesterol, triglycerides and thyroxine, and thyroid weight. To elucidate the possible impact of exogenous iodine on impaired free radical tissue defense mechanisms STZ-diabetic rats were exposed to iodine brine providing for a daily iodide uptake of about 300 micrograms/kg body weight. STZ-exposure caused a decline in thyroid weight (p less than 0.01) and in total serum thyroxine (p less than 0.001), as well as a fall in hepatic catalase (CAT) activity (p less than 0.01) versus control group. Impairment of catalase activity was related to serum glucose level (r = -0.569, p less than 0.01), while hepatic MDA was positively related to serum glucose (r = + 0.5, p less than 0.01). No protective effects of iodine brine were seen with regard to impairment by STZ of antioxidant enzyme status. We conclude that impairment by STZ of antioxidant enzymes may contribute to STZ-dependent experimental diabetes.
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PMID:Alterations of antioxidant tissue defense enzymes and related metabolic parameters in streptozotocin-diabetic rats--effects of iodine treatment. 150 40

The effects of sodium orthovanadate (0.6 mg/ml in drinking water) on hexokinase isozymes, pyruvate kinase and malic enzyme in liver and kidney of control and alloxan diabetic rats were studied and compared. Vanadate treatment of diabetic rats normalized hyperglycemia and almost completely restored the differentially altered enzyme profile of liver (a tissue that underutilizes glucose in diabetes) and kidney (a tissue that overutilizes glucose during diabetes). Vanadate therapy, however, could not restore the depressed plasma insulin level of diabetic rats. The study clearly indicates that vanadate can effectively normalize many metabolic abnormalities even at a low insulin level in both insulin-dependent and -independent tissues of diabetic rats.
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PMID:Effects of vanadate on glycolytic enzymes and malic enzyme in insulin-dependent and -independent tissues of diabetic rats. 152 51


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