Home Remedies for Hyperglycemia

Blood Sugar Miracle

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Blood Sugar Miracle Overview


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Supportive Therapeutics

The exact dose of steroids necessary for each patient will vary depending on the histology (i.e., benign or malignant), size and location of the tumor, and amount of peritumoral edema. In general, most patients with malignant tumors will require between 8 and 16 mg of dexamethasone per day to remain clinically stable. The lowest dose of steroid that can control the patient's pressure-related symptoms should be used 1,21 . This approach will minimize some of the toxicity and complications that can arise from long-term corticosteroid usage, which includes hyperglycemia, peripheral edema, proximal myopa-thy, gastritis, infection, osteopenia, weight gain, bowel perforation, and psychiatric or behavioral changes (e.g., euphoria, hypomania, depression, psychosis, and sleep disturbance) 1,27-31 . Patients with dexa-methasone-induced proximal myopathy will often improve when the dosage is reduced 30,31 . In addition, the proximal leg muscles can usually be strengthened if the patient is...

Characteristics of an Animal Model Modeling Pathology or Function

Animal models of human disease are seldom comprehensive. Rarely does a single system recapitulate all aspects of the human pathological process. Defining the key characteristics of a disease to be reproduced requires some knowledge of the driving force for the pathology and the symptoms. Secondary co-morbid characteristics that may be observed in the disease, but that are not critical for disease progression, would clearly be poor choices for modeling. It is not always easy to tell the difference. Before the development of molecular targets and mechanism-based approaches, pharmaceutical research and drug discovery were heavily based on animal models that reproduced symptoms seen in humans. Animals with high blood pressure or hyperglycemia were treated to determine which compounds best normalized the condition. The success of such models in predicting efficacious agents in humans depended greatly on whether the mechanisms were similar.

Further Clinical Aspects

When the blood glucose rises to relatively high levels, the kidney also exerts a regulatory effect. Glucose is continuously filtered by the glomeruli but is normally completely reabsorbed in the renal tubules by active transport. The capacity of the tubular system to reab-sorb glucose is limited to a rate of about 350 mg min, and in hyperglycemia (as occurs in poorly controlled diabetes mellitus) the glomerular filtrate may contain more glucose than can be reabsorbed, resulting in glu-cosuria. Glucosuria occurs when the venous blood glucose concentration exceeds 9.5-10.0 mmol L this is termed the renal threshold for glucose.

Protease inhibitors PIs

All protease inhibitors can be used in combination with 2 NRTIs. PIs differ from each other in respect to their tolerability and side effects. As with adults, dyslipide-mia is associated with the use of protease inhibitors (Lainka 2002). It includes elevated total cholesterol, triglycerides (TG), and low density lipoprotein cholesterol (LDL-c) and decreases in high density lipoprotein cholesterol (HDL-c) In lipodys-trophy, there is a loss of subcutaneous fat (lipoatrophy) and or a deposition of fat tissue subcutaneously or in visceral stores (lipohypertrophy) including the presence of dorsocervical fat accumulation (buffalo hump) and increased waist-to-hip ratio. Lipoatrophy is marked by thinning of subcutaneous fat in the face, buttocks, and extremities associated with a prominent appearance of peripheral veins. The body habitus changes usually occur gradually over months to years. The exact prevalence of lipodystrophy in children is unknown and there are no clear diagnostic...

Dexamethasone Decadron

Adverse effects delayed wound healing, seizures, osteoporosis, hyperglycemia, diarrhea, nausea, GI bleeding, cushingoid effects. Comments use with caution in patients with hypothyroidism, cirrhosis, hypertension, CHF, ulcerative colitis, thromboembolic disorders may cause adrenocortical insufficiency (Addison's crisis) with abrupt withdrawal.

Biological And Molecular Actions

Insulin is the chief hormone controlling intermediary metabolism. It affects virtually every tissue in the body, but principally liver, muscle, and adipose tissue. Its short-term effects are to reduce blood glucose and to conserve body fuel supplies. There are also a number of effects of insulin on the regulation of gene transcription and cell replication. Thus, an understanding of the mode of action of insulin is complex Figure 728 presents an introductory schematic diagram of the signal transduction events that link the formation of an insulin-receptor complex to the generation of its many biological responses.

Clinical Aspects

The major pathophysiological abnormalities generated by diabetes mellitus include the following (i) glucose intolerance or inappropriately high blood glucose levels in the presence of elevated or normal insulin concentrations (ii) acidosis and ketosis (iii) reduction of the enzymes for gluconeogenesis (iv) reduced growth (v) a microangiopathy, including a thickened basement membrane of capillaries in muscle and retinal blood vessels and of the capillaries of the renal glomerulus and (vi) a neuropathy, including peripheral sensory and motor defects.

Of Postmortem Chemical Data

The most important changes of body-fluid components after death are compiled in Table 11-1. A synopsis of postmortem chemical findings in diseases such as diabetes mellitus is shown in Table 11-2. The tables show that glucose is best determined in vitreous because blood glucose values may increase dramatically in the agonal period, particularly after resuscitation attempts (1). Hyperglycemia and diabetic ketoacidosis can be diagnosed readily but hypoglycemia cannot be confirmed by postmortem testing. The dehydration pattern (Table 11-2) has provided a compelling basis for the diagnosis of dehydration in cases of homicidal deprivation of food and water.

Clinical Considerations

It is characterized clinically by hyperglycemia, ketoacidosis, and exogenous insulin dependence. Long-term clinical effects include neuropathy, retinopathy leading to blindness, and nephropathy leading to kidney failure. b. Routine screening often detects hyperglycemia, or patient complaints of polyuria lead to detection of type 2 diabetes. (2) Hyperinsulinemia is present, but postprandial hyperglycemia is observed.

The intrauterine diabetic environment an intrauterine teratogenic milieu

The exact mechanism behind the teratogenicity of the maternal diabetic state is poorly understood but tight glycemic control has been correlated with improved neurodevelopment (Sells et al., 1994) and fewer structural malformations (Ray et al., 2001) implying that maternal hyperglycemia or factors associated with it are responsible.

Octreotide Sandostatin

Dose (ped) 1-10 mcg kg every 12 hrs beginning at low end of range and increasing by 0.3 mcg kg dose at every 3 days max dose 1500 mcg 24 hr. Clearance hepatic and renal. Adverse effects may cause nausea, decreased GI motility, transient hyperglycemia, cholelithiasis, abdominal discomfort, headache, pain at injection site growth hormone suppression with long term use. Comments cyclosporine levels may be reduced.

Embryonic Stem and Primordial Germ Cells Are Pluripotent

(EB) induces the differentiation of neural, dopaminergic, and glial elements (Brustle et al., 1999 Kim et al., 2002 Schuldiner et al., 2000), and insulin-secreting cells (Assady et al., 2001 Lumelsky et al., 2001), among others. Although the results in the mouse were not perfect (transplantation of the insulin-secreting cells did not produce a sustained correction of hyperglycemia in the engrafted animals), the islet-like clusters survive and secrete insulin in vivo. Other tissues generated from ES cell lines include mouse and human cardiomyocytes (Kehat et al., 2001 Maltsev et al., 1993 Wobus et al., 1997), hematopoietic cells (Kaufman et al., 2002 Nakano et al., 1996 Wiles et al., 1991), endothelial cells (Risau et al., 1988 Yamashita et al., 2000), skeletal muscles (Miller-Hance et al., 1993 Rohwedel et al., 1994), chondrocytes (Kramer et al., 2000), liver (Hamazaki et al., 2001), neural cells (Carpenter et al., 2001 Reubinoff et al., 2001 Zhang et al., 2001), and adipocytes (Dani...

Heterologous Regulation of IRSProtein Signals

Various cytokines or metabolites promote serine phos-phorylation of the IRS-proteins which inhibits signal trans-duction and causes insulin resistance. Adipose-derived cytokines, especially tumor necrosis factor alpha (TNFa), inhibit signaling by serine phosphorylation of IRS1 IRS2 76-78 . The signaling cascades regulated by TNFa are complex and involve many branch points, including the activation of various serine kinases and transcription factors that promote apoptosis or proliferation 79 . Inhibition of IkB kinase (IKKP) with high doses of salicylates reverses hyperglycemia, hyperinsu-linemia, and dyslipidemia in obese rodents by sensitizing the insulin signaling pathway 80,81 . Although no physical interaction occurs between IRS-proteins and IKKP, salicy-lates increase insulin-stimulated tyrosine phosphorylation of the IRS-proteins in the liver, suggesting that IKKP might indirectly inhibit insulin receptor function or its coupling to the substrates 82 .

Regulation Of Islet Activity

Some amino acids also stimulate insulin secretion, either alone or in concert with elevated blood glucose levels. Increased blood fatty acid levels also stimulate insulin release, as do circulating gastrin, CCK, and secretin. CCK and glucagon, released in the islet by the A cells, act as paracrine secretions to stimulate B cell secretion of insulin.

Pathogenesis of Diabetes Mellitus Type 2 in Relation to Aging

This means a reduction in the activity of insulin on its target tissues such as muscle, liver, and adipose tissue. In the muscle this results in a decrease of glucose disposal. In the adipocytes this results in the inability of insulin to inhibit the lipolysis leading to the release of free fatty acids in the circulation. These FFAs in turn stimulate hepatic neoglucogenesis and VLDL secretion, reduce muscle glucose uptake, and may alter glucose-stimulated insulin secretion by beta cells. This age-related impairment of insulin action appears to be predominantly due to effects on the insulin signaling mechanism beyond the insulin receptor itself. However, the latter also may be involved to some extent (Fulop et al., 2003). In the liver the resistance results in the inadequate suppression of the endogenous glucose production even in the presence of hyperglycemia. The gold standard technique for measuring the insulin resistance in humans is the...

Pancreatic Beta Cell Dysfunction

The pancreatic beta cell dysfunction seen with aging is associated with alterations of glucose-stimulated insulin pulse mass, kinetics, and rhythmicity. Normally, insulin is secreted in a pulsatile manner that insures a higher sensitivity at the receptor level and lower needs for secretion. This pulsatile secretion is controlled by the oscillation of the intra-cytoplasmic calcium level. In type 2 diabetes, there is an over-activity of plasma membrane KATP-channel due to chronic hyperglycemia altering electrical activity by Ca2+ and consequently the insulin secretion. With aging, calcium metabolism was shown to be altered in various cell types thus it is plausible that this also occurs in pancreatic cells. Moreover, if intracellular calcium concentration remains high, this could result in the apoptosis of pancreatic cells, potentially contributing to the significant 20 to 40 reduction of beta cell mass associated with type 2 diabetes. Thus, a tight control of calcium metabolism is...

Relationship between Diabetes Mellitus and Aging in the Development of Cardiovascular Diseases

Development of atherosclerosis, as it is also for type 2 diabetes. Aging per se could present a state of impaired glucose tolerance due to the physiologic changes described. IGT is known to be a risk factor for progression to type 2 diabetes. Aging associated with the occurrence of type 2 diabetes increases several-fold the risk for development of cardiovascular diseases by approximately six to eight times more than aging alone (Nesto, 2003). This is due mainly to the strong occurrence of the classical, including hypertension, dyslipidemia, and nonclassical, including inflammatory cytokines, homocystein, and CRP risk factors. Altogether, the common pathway could be the insulin resistance and insulinopenia-induced hyperglycemia via the production of AGEs and oxidative stress.

Cardiovascular Disease

The main cause of reduced life expectancy in diabetes is the increased incidence of cardiovascular disease (CVD) (Mooradian, 2003). Although the cause of accelerated ath-erogenesis in diabetes is mostly the result of increased prevalence of comorbidities such as obesity, hypertension, and dyslipidemia, it appears that hyperglycemia and possibly hyperinsulinemia or relative insulin deficiency have an important role.

Neurobehavioral Changes

That insulinization and reducing hyperglycemia ameliorates cognitive deterioration (Flood et al., l990). Nevertheless, some of the changes in the central nervous system (CNS) function in diabetes are the result of cerebrovascu-lar accidents and as such are not readily reversible with control of blood glucose levels.

Pathogenic Mechanisms

The blood flow from visceral fat depot is drained via the portal vein to the liver, in contrast to other fat depots that are drained to the systemic circulation. Visceral adipose tissue has a higher turnover rate of fat, in both men and women, than other adipose tissue depots (11). Both lipid accumulation, by the action of lipoprotein lipase (LPL), and the lipolytic response to catecholamines are elevated (11-13). The increased lipolytic activity of visceral fat combined with its anatomical localization means that the liver is exposed to higher concentrations of free fatty acids (FFA) than any other organ. FFA have important influence on the liver metabolism. Increased levels of FFA attenuates the hepatic clearance of insulin from the pancreas and enhances the gluconeogenesis and the secretion of very low density lipoproteins (VLDL) from the liver (14-17). Therefore, with enlarged visceral adipose tissue depots, as in visceral obesity, these effects of FFA on the liver would be...

Mechanisms of Premature Aging in Diabetes

The clinical and phenotypic similarities between aging and diabetes suggest that there may be shared biochemical pathways leading to the tissue changes. Glucose is the principal metabolic fuel for many animal species. In general, with few exceptions, the plasma glucose level in various animals is maintained within a narrow range (60-140 mg dl). It is possible that the lower limit of blood glucose levels is determined by the minimum tissue requirements of metabolic fuel, and the upper limit defines the threshold beyond which glucotoxicity limits survival of the species (Mooradian and Thurman, 1999b). Avian species, especially owls and parrots, are the exception to this generalization. These animals have high blood glucose levels in the range of 250 to 350 mg dl and yet have a relatively long life expectancy and show no signs of classical diabetic complications. The overall constancy of blood glucose levels across a wide range of animal species suggests that hyperglycemia, except in...

Protein Kinase C Activation

In recent years, protein kinase C has emerged as a potential target for therapeutic agents that reduce the risk of complications in diabetes. PKC is a calcium-dependent enzyme involved in signal transduction through changes in the phosphorylation of key cellular proteins. High blood glucose levels increase phospholipase D activity, which in turn, activates the membrane-bound PKC. This activation accounts at least in part for the increased cell permeability and vascular resistance. In pathological state of hyperglycemia, diacylglycerol (DAG) content is increased, which along with the increased oxidative Hyperglycemia

GSK3 as a Drug Target

Insulin induces the activation of glycogen synthase, mainly by stimulating the dephosphorylation of the serine residues in glycogen synthase that are targeted by GSK3 27 and stimulates the activation of eIF2B by promoting the dephosphorylation of Ser535 9 . These dephosphorylation events, which are likely to be mediated (at least in part) by the PKB-catalyzed inhibition of GSK3, contribute to the insulin-induced stimulation of glycogen and protein synthesis. For these reasons, and because the level of GSK3 is elevated in animal models of diabetes 28 , there has been considerable interest over the past few years in trying to identify GSK3 inhibitors for the treatment of Type 2 diabetes. Small-cell-permeant inhibitors of GSK3 have now been developed. These are relatively specific and can activate glycogen syn-thase and stimulate the conversion of glucose to glycogen in liver cells 29 . Related compounds have also been reported to lower blood glucose levels in vivo 30 . The efficacy of...

Putative Mechanisms Underlying Interactions Between Somatotropic Axis And Sleep

There is evidence that, under physiological conditions, sleep-related GH secretion may be less sensitive to somatostatin inhibition than spontaneous daytime GH secretion or daytime GH secretion in response to a variety of stimuli. Indeed, during sleep, GH secretion is not suppressible by acute hyperglycemia (129), a potent mechanism of inhibition of daytime GH release mediated in part by increased hypothalamic somatostatin activity. Similarly, aging, which is thought to be associated with a progressive increase in somatostatinergic tone (130), seems to affect GH secretion less during sleep than during wake, as the secretory output associated with the sleep-onset GH pulse remains relatively preserved (77). Reductions in somatostatinergic tone achieved by pharmacological treatment will generally enhance sleep-related GH secretion in adults (128,131) but in children, such treatments affect daytime, but not nocturnal, GH release because hypothalamic somatostatin activity is thought to be...

Blood Glucose Is Derived From The Diet Gluconeogenesis Glycogenolysis

Liver Glut Transporter Bidirectional

In addition to the direct effects of hyperglycemia in enhancing the uptake of glucose into the liver, the hormone insulin plays a central role in regulating blood glucose. It is produced by the B cells of the islets of Langerhans in the pancreas in response to hyper-glycemia. The B islet cells are freely permeable to glu- cose via the GLUT 2 transporter, and the glucose is phosphorylated by glucokinase. Therefore, increasing blood glucose increases metabolic flux through glycolysis, the citric acid cycle, and the generation of ATP. Increase in ATP inhibits ATP-sensitive K+ channels, causing depolarization of the B cell membrane, which increases Ca2+ influx via voltage-sensitive Ca2+ channels, stimulating exocytosis of insulin. Thus, the concentration of insulin in the blood parallels that of the blood glucose. Other substances causing release of insulin from the pancreas include amino acids, free fatty acids, ketone bodies, glucagon, secretin, and the sulfonylurea drugs tolbutamide...

Human Studies On Agerelated Cataracts

The GALK1 results fit in well with the known influence of hyperglycemia on age-related cataracts. That these cataracts result from polyol accumulation is suggested by work in galactosemic dogs and transgenic and knockout mice. Dogs have aldose reductase levels similar to those in humans and when stressed readily develop sugar cataracts that are prevented by aldose reductase inhibitors. Mice, which have very low aldose reductase activity in the lens, are naturally resistant to sugar cataracts, either galactosemic or hyperglycemic. However, upon transgenic expression of aldose reduc-tase, mice readily develop cataracts, especially when the galactokinase or sorbitol dehydrogenase gene is deleted. Consistent with these animal data are the recent findings that susceptibility to cataracts as a diabetic complication in humans is associated with specific allele Z of the

Myoblasts and Gene Therapy

The transplantation of genetically-engineered myoblasts, or the transduction of muscle fibers, provides the possibility of therapy for non-muscle diseases. The transplantation of C2C12 cells engineered to express insulin in diabetic mice, for example, resulted in the development of insulin producing and secreting myofibers 204 . These mice showed significantly increased insulinemia and decreased hyperglycemia.

Dose treatment of drug extravasation

Adverse effects may cause nystagmus, diplopia, ataxia, drowsiness, gingival hyperplasia, gastrointestinal upset, hyperglycemia, hirsutism, SLE-like and Stevens-Johnson syndromes IV form may cause hypotension, arrhythmias, bradycardia, cardiovascular collapse, CNS depression, respiratory arrest, venous irritation and pain. Comments induces hepatic microsomal enzymes crosses the placenta significant interpatient variation in dose needed to achieve therapeutic concentration use caution in renal and hepatic impairment. Dose (ped) 0.1-2 mg kg day IV IM PO (as sodium phosphate salt) in divided doses 1-4 times day. Clearance renal elimination. Adverse effects insomnia, nervousness, indigestion, hirsutism, hyperglycemia, diarrhea, HPA axis suppression.

Angleclosure Glaucoma

Glycerol is administered as a liquid in dosages of 1 to 1.5 g kg of body weight,3 either as a 100 solution mixed with an equal volume of iced juice or as a commercial preparation (Osmoglyn, 50 solution). Oral glycerol is rapidly absorbed, is distributed throughout the extracellular water, and penetrates the eye poorly. The drug is metabolized by the liver rather than excreted by the kidneys, producing less diuresis than do other hyperosmotic agents. Glycerol has an unpleasantly sweet taste and may cause vomiting. The caloric content is 4.32 cal g, which, combined with the osmotic diuretic effect and resultant dehydration, mandates special caution when used in diabetic patients, who may develop hyperglycemia and ketosis.4

Heart Disease A Cardiologists POV

Summary This article, written by a cardiologist with a family history of diabetes, discusses the personal events that led to his interest in the cardiovascular effects of diabetes. The article begins with the author's recollections of his family's attitude about his grandfather's diabetes. This is followed by an account of his father's problems with high blood glucose and its effects on his heart. In addition, the author recounts his own experience with the effects of high blood glucose, its effects on his body, and his realization of the connection between diabetes and heart problems.

Pharmacological Treatment of the Paraphilias

Methoxyprogesterone acetate (MPA) is the most commonly used hormonal agent for the reduction of sex drive in the United States (140,146,154,155). It does not compete with androgens at the receptor level but blocks levels of testosterone by inducing hepatic testosterone reductase. The goal of this strategy is to reduce baseline testosterone to 50 of initial values. Common dosages are 50-300 mg orally or 300-400 weekly via intramuscular injections with reduction to 100 mg weekly for a maintenance program. Depot preparations of methoxyprogesterone are also available. Side-effects include weight gain, hyper-glycemia due to an exaggerated insulin response to a glucose load, headaches and increased risk of deep vain thromboses.

Stem Cells Of The Spleen

Although the onset and progression of Type I diabetes can be managed through intensive insulin therapy, this type of therapy does not liberate the patient from insulin dependence. Restoring -cell function through regenerating -cells from islet cell precursors is an attractive alternative to transplantation of exogenous -cells. Problems with scarcity of material and immunological rejection are circumvented by the use of embryonic stem (ES) cells, which can differentiate into a variety of cell lineages in vitro. Soria et al. made use of a cell-trapping system to generate an insulin-secreting cell clone from undifferentiated ES cells (Soria et al., 2000). ES-implanted animals reached a normalized weight by four weeks postimplantation, and implantation led to correction of hyperglycemia within one week. ES-derived insulin-containing cells are able to normalize blood glucose in diabetic mice, but using this technology in human therapies involves first solving problems with ES cell use,...

Neonatal Transient Diabetes Mellitus

Neonatal transient diabetes mellitus (TNDM), with an incidence in newborns of 1 400,000 to 1 500,000 (Fosel, 1995 Shield et al., 1997), is characterized by intrauterine growth retardation, failure to thrive, hyperglycemia, glucosuria, dehydration, polyuria, occasional ketonemia and ketonuria, lethargy, and fever. Occasional features include anemia, macroglossia (Figure 1), and umbilical hernia. The diabetic condition may be permanent, subside to recur later as type 2 diabetes (Shield et al., 1997), or vanish completely (Christian et al., 1999).


Three systemic reviews of herbal medicines for glycaemlc control In diabetes found that Aloe vera can lower blood glucose levels In diabetic patients (Grover et al 2002, Vogler & Ernst 1999, Yeh et al 2003). In one trial aloe juice consisting of 80 gel or placebo was given In a trial of 40 patients who were recently diagnosed with type 1 diabetes at the dose of 1 tablespoon twice dally. From day 14 the blood sugar levels In the aloe group began to fall significantly compared with the control group and Aloe vera 27


A further patient who presented at birth with transient neonatal diabetes mellitus (TNDM) and paternal UPD6 was described (Christian et al., 1999). This child presented with low birthweight, macroglossia, hypertelorism, and club foot in addition to neonatal diabetes (see Figure 1, Chapter 5). Hyperglycemia was transient, and insulin treatment was discontinued at 4 months of age. Analysis with polymorphic DNA markers for chromosome 6 indicated the presence of paternal UPD6. The authors discussed that there were three cases with paternal UPD6 that also included additional anomalies, such as macroglossia. Therefore, the simultaneous finding of NDM and macroglossia should be a strong indicator for genetic testing (Christian et al., 1999).

Endocrine Effects

Curve (AUC) was increased approx 20 whereas C-peptide AUC was increased approx 70 . In a follow-up study in noninsulin-dependent patients with diabetes mellitus who received the same 3-month GB therapy, following an oral glucose tolerance test, a blunted plasma insulin response was noted, leading to a reduction in insulin AUC (38). Conversely, C-peptide levels were increased, leading to a dissimilar insulin C-peptide ratio. The author suggested this indicated an increased hepatic extraction of insulin relative to C-peptide, potentially resulting in reduced insulin-mediated glucose metabolism and elevated blood glucose.


Steroid side effects have been well defined over time and usually worsen with higher dose and longer duration of use. Side effects include weight gain, electrolyte disturbances, hyperglycemia, gastrointestinal irritation, osteoporosis, opportunistic infections (primarily Can


There are two groups of drugs that when given orally, are capable of effecting a sharp drop in the elevated blood glucose levels associated with diabetes (see Figure 7-27). These are the sulfonylurea derivatives (tolbutamide, chlorpropamide, glibenclamide, tolazamide, and glipizide) and the biguanide derivative (phenformin). When these oral drugs were first introduced in the early 1960s, there was much hope that they would provide a long-term solution to the management of diabetes. However, their general use has

Ketone Bodies

Diabetic ketoacidosis is a clinical condition characterized by hyperglycemia, hyperketonemia, and concomitant metabolic acidosis that largely results from elevated blood levels of 3-hydroxybutyrate and acet-oacetate. A propensity to diabetic ketoacidosis is the primary basis for clinical classification of a subject with juvenile-onset diabetes. The clinical symptoms arise from a low-to-undetectable blood level of insulin and result in the adverse consequence of persistent hyperglycemia. In the extreme, an afflicted subject will become unconscious due to diabetic coma. Diabetic ketoacidosis is an acute life-threatening emergency and if left untreated leads to hypokalemia and cardiovascular failure. Diabetic ketoacidosis accounts for 65 of all diabetic hospital admissions in the age group 1-20 years and 40 in the 21-34-years age group. glucose signals (i.e., the 3-cells are still functioning). It is frequently not diagnosed until the individual is middle-aged. In this form of the...

For 3 days Dose ped

Acute spinal cord injury 30 mg kg IV over 15 minutes, followed in 45 minutes by a continuous infusion of 5.4 mg kg hr for 23 hrs. Clearance hepatic metabolism renal elimination. Contraindications serious infections except septic shock or tuberculous meningitis. Adverse effects may cause hypertension, pseudotumor cerebri, acne, Cushing's syndrome, adrenal axis suppression, GI bleeding, hyperglycemia, and osteoporosis. Comments use caution in hyperthyroidism, cirrhosis, nonspecific ulcerative colitis, hypertension, osteoporosis, thromboembolic tendencies, CHF, convulsive disorders, myasthenia gravis, thrombophlebitis, peptic ulcer, diabetes.

Diabetes Mellitus

Following a 4-wk period of intensive insulin and dietary intervention to improve glycemic control in six adolescents with poorly controlled IDDM, there was no change in the mean 24-h GH concentration, pulse frequency or amplitude. Serum IGF-I concentrations improved significantly, reflecting improved GH sensitivity and partial correction of a GH resistance-like state (37). Enhanced GH secretion in the face of chronic hyperglycemia and following GHRH administration appears consistent with a state of diminished somatostatin tone in subjects with diabetes (37).


Hyperglycemia as a hallmark of diabetes mellitus, in turn, is known to contribute directly to insulin resistance as well as potentially interfering with normal pancreatic cell function, thereby setting the stage for a vicious circle of maladaptative mechanisms. Hyperglycemia, through the deregulation of KATP-channel, exerts a toxic effect on insulin secretion via the intracellular Ca2+ oscillation mediated by voltage-gated channels. The exposition of beta cells to chronic hyperglycemia as well as free fatty acids alter the insulin secretion induced by glucose. During the formation of AGEs as well as during their interaction with RAGEs, free radicals are produced. Thus, free radicals not only were implicated as a cause and a consequence of the aging process, but also as a consequence of hyperglycemia. AGEs as well as free radicals may directly influence or interfere with the insulin receptor (IR) function and signal transduction by diminishing the tyrosine phosphorylation of IRS1 2,...

B Ginseng

There are three species of ginseng in common use in the United States American ginseng, Korean ginseng, and Siberian ginseng. All are regarded as adaptogens that normalize immune functions and are preparations that help the body adapt to change, thus lowering the risk of stress-related illness. American ginseng, whose botanical name is Panax quinquefolius, has recently been evaluated as a treatment for high blood sugar in patients with type 2 (adult-onset) diabetes. It is considered to be less stimulating than the Korean or Siberian varieties. Korean

Neoplastic Disease

There are additional hypothetical causes for increased carcinogenesis in diabetes. Type 2 diabetes mellitus may be associated not only with the elevated level of oxidative DNA damage, but also with the increased susceptibility to mutagens and the decreased efficacy of DNA repair (Blasiak et al., 2004). Protein kinase B (PKB) is implicated in glucose metabolism and in the regulation of apoptosis and is activated by insulin, which may partially explain why PKB is over-expressed in some ovarian, breast, and pancreatic carcinomas (Galetic et al., 1999). Inflammatory markers are increased in diabetes. Elevated CRP levels are a strong independent predictor of type 2 diabetes and may mediate associations of TNF-alphaR2 and IL-6 with type 2 diabetes (Hu et al., 2004) (Spranger et al., 2003). Finally, the role of hyperglycemia in carcinogenesis could include pathways related to luminal factors such as fecal bile acid concentrations, stool bulk, and prolonged transit time, or glucose could be...

Oxidation Pathway

There is some controversy regarding whether uncontrolled hyperglycemia in diabetes causes increased free radical generation or whether the increased presence of oxidized proteins and lipids is the result of defective clearance of these byproducts (Hasanain and Mooradian, 2002 2004). Nevertheless, there is extensive evidence in human subjects, in various animal models of diabetes, and in cell culture studies that hyperglycemia is associated with reduced antioxidant defense capacity, and increased accumulation of oxidation byproducts. In nuclear and mitochondrial DNA, 8-hydroxydeoxyguanosine (8-OHdG), an oxidized nucleoside of DNA, is the most frequently detected and studied DNA lesion. Elevated urinary 8-OHdG and leukocyte DNA were also detected in diabetic patients with hyperglycemia, and the level of urinary 8-OHdG in diabetes correlates with the severity of diabetic nephropathy and retinopathy (Wu et al., 2004). The increased superoxide generation is more closely related to...


The number of people with diabetes (most of it T2D) is expected to double in a generation, from 150 million in 2000 to 300 million by 2025 (Zimmet et al., 2001). As many as one-in-ten of the people alive on the planet today will develop diabetes during their lifetime. Many hundreds of millions more will have modestly elevated blood glucose levels, which, although they do not constitute frank diabetes, are nevertheless associated with a heightened risk of cardiovascular disease (Alberti, 1996 Perry and Baron, 1999).

Diabetes Assessment

Diabetes affects millions of people worldwide. It is a leading cause of death, and as a result, is a large area of study. Diabetes is actually a group of diseases characterized by aberrant glucose metabolism. Type I or insulin-dependent diabetes results from immune-mediated destruction of pancreatic beta-cells. Type II or noninsulin-dependent diabetes results in hyperglycemia without loss of endogenous insulin reserve or loss of pancreatic islets. Thus, Type II diabetes is characterized by the presence of insulin resistance, which is often associated with obesity and advancing age and accounts for most cases of diabetes. The use of mouse models and transgenic technology has been important in the understanding of this complex disease.42


History of the Present Illness Potassium < 3.5 mMol L (repeat test to exclude lab error), hyperglycemia, diuretics, diarrhea, vomiting, laxative abuse poor intake of potassium containing foods (fruits, vegetables, meats) . Conn's syndrome (hyperaldosteronism). Urine potassium.


Maintenance of optimal cerebral perfusion pressure is critical (maintaining normal arterial blood pressure, intracranial pressure, oxygen carrying capacity, arterial oxygen tension and hematocrit maintained 30-34 ). Hyperglycemia aggravates neurologic injuries and should be avoided.

Brief Overview

Brief epidemiology of age-related cataracts Age-related cataracts are associated with a number of environmental risk factors, including cigarette smoking or chronic exposure to wood smoke, obesity or elevated blood glucose levels, poor infantile growth, exposure to ultraviolet light, and alcohol consumption (The Italian-American Cataract Study Group, 1991). Conversely, antioxidant vitamins seem to have a protective effect, although this has not been borne out by all studies.

Infection Fungal

Candida albicans is a common organism found in the oral cavity flora that causes candidiasis in certain clinical situations. Candida has a capsule and forms true hyphae and pseudohyphae. It adheres to mucosal surfaces and is capable of superficial mucosal invasion. Factors that contribute to oral candida proliferation include uncontrolled diabetes mellitus, antibiotic therapy, and any condition that causes immunosuppression. Clinical features of candidiasis include white, cheesy plaques that can be wiped off with a tongue blade. The tongue and buccal mucosa are frequently infected, but tonsillar and pharyngeal lesions are not uncommon and may extend to the esophagus and larynx. Superficial infections are often painless and self-limiting. Deep infections can cause ulcerative lesions that are painful. Diagnosis is made by epithelial scrapings and KOH preparations demonstrating budding yeast and hyphae under light microscopy. Cultures may be obtained if needed. Treatment of...


Intravascular absorption of irrigating fluid the amount of solution absorbed depends on the hydrostatic pressure of the irrigating fluid, the duration of time sinuses are exposed to irrigating fluid (10 to 30 mL of irrigating fluid is absorbed per minute), and the number and sizes of the venous sinuses opened during resection. Absorption of the irrigating fluid can result in fluid overload, serum hypoosmolality, hyponatremia, hyperglycemia, hyperammonemia, hemolysis.

Type I Diabetes

The characteristic dysfunction is the destruction of pancreatic beta cells that produce insulin. This results clinically in hyperglycemia, ketoacidosis, and exogenous insulin dependence. Long-term clinical effects include neuropathy, retinopathy leading to blindness, and nephropathy leading to kidney failure.

Risk Factors

The risk of mortality and morbidity from stroke in subjects with diabetes is increased by more than two-fold diabetes is an independent risk factor for stroke (Mankovsky and Ziegler, 2004). Chronic hyperglycemia, insulin resistance, and their associated cellular and molecular alterations may contribute to an elevated stroke risk either by amplification of the harmful effect of existing risk factors or by acting independently. The pathophysiological and biochemical ischemic cerebral impairments in patients with diabetes are not fully characterized however, as the risk of morbidity and mortality associated with stroke in patients with diabetes

Otic Diseases

Malignant otitis externa, also termed necrotizing otitis externa, is a skull-based osteomyelitis of otogenic origin. Patients present with severe otalgia, otorrhea, and cranial neuropathies. The facial nerve is the most common cranial nerve involved with studies ranging from 24 to 43 (74). The usual pathogen is Pseudomonas aeruginosa and often occurs in immunocompromised patients, typically with diabetes mellitus. Diagnosis is clinical, with an elevated sedimentation rate characteristic on serum evaluation (75). Patients also display increased tracer uptake on technetium or gallium nuclear medicine scans. Treatment requires aggressive blood sugar control and long-term antibiotic therapy directed toward P. aeruginosa. Hyperbaric oxygen has also proven beneficial in treating the chronic osteomyelitis. Prognosis is guarded, with mortality near 20 (74). Facial nerve recovery is also reported as quite poor in the literature, with little or no recovery of function,...

Agerelated cataract

Fovea Blood Pressure

Which is found exclusively in Japanese and other eastern populations, is present in 8 of Japanese with age-associated cataract compared with 4 of the general population (P< 0.02)(0kano et al., 2001). Diabetes mellitus is a known risk factor for cataract, which here also results from polyol accumulation. Hyperglycemia results in greatly increased glucose uptake in tissues where uptake is independent of insulin, including lens, retina, kidney and peripheral nerves (Harding, 1991). As a result, the glucose flux through the polyol pathway is increased tenfold. The excess glucose is reduced by aldose reductase to sorbitol, which accumulates and becomes hydrated in lens fibres and epithelium, leading to osmotic stress, a major factor in diabetic cataract. Susceptibility to diabetic cataract has been associated with a specific polymorphism upstream of the aldose reductase gene (Lee et al., 2001), although this remains to be replicated. Finally, common variation in the...

Case 5

This was the report of a further patient with TNDM and paternal UPD6 (Whiteford et al., 1997). The term-born infant was growth-retarded, with weight, length, and occipitofrontal circumference below the 3rd centile. Insulin infusion was started on the first day, after hyperglycemia and hyperglucosuria were noted subcutaneous injections were given after 2 weeks, insulin requirements decreasing by 6 weeks and discontinued at 8 weeks of age. Imaging, by ultrasound and computerized tomography, twice failed to reveal pancreatic tissue, but stool chemotrysin activity (from exocrine glands) and glucagon (from alpha-cells) had been tested as normal and, at 14 weeks, a pancreas of normal size was visualized. At 7 months, weight and length were at the 3rd centile, with head

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