Home Remedies for Hyperglycemia

Blood Sugar Miracle

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Insulin Resistance and Hyperglycemia

The WHO definition of the metabolic syndrome is the only one that utilizes a measure of insulin resistance as a required component, although elevated fasting glucose levels, specified by the ATP III and IDF definitions, are often associated with an insulin-resistant state. Insulin resistance can be defined as the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle, and liver cells. In mild cases of insulin resistance, increased insulin secretion by pancreatic P cells results in hyperinsulinemia to maintain eug-lycemia. As insulin resistance worsens, individuals whose increased pancreatic insulin secretion is unable to compensate for the reduced insulin action develop impaired glucose tolerance and hyperglycemia.

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.

Project Title Calcium Regulation In The Diabetic Heart

Summary Heart disease is the leading cause of death in diabetic patients, and considerable evidence is now available to support the existence of a specific diabetic cardiomyopathy that is independent of coronary artery disease and hypertension. Functional and biochemical data acquired from multicellular cardiac preparations of diabetic animals support the view that cellular mechanisms controlling cytosolic Ca2+ on a beat-to-beat basis are abnormal and contribute to impaired relaxation. The goal of this project is to characterize diabetes-induced changes in the expression and function of Ca2+ regulating proteins in isolated cardiac myocytes, and to determine the role of hyperglycemia in the pathogenesis and pathophysiology of diabetic cardiomyopathy. To test the hypothesis that abnormal Ca2+ handling occurs at the single cell level, biophysical assessment of excitation-contraction coupling will be carried out in ventricular myocytes isolated from diabetic rats. Voltage clamp techniques...

Take Advantage of the Technology

Jessica, a student of physiology, is constantly drinking from a water bottle yet claims to be constantly thirsty. During her physiology laboratory exercise involving urinalysis, she discovers that she has a significant amount of glucose in her urine. Alarmed, because urine normally should contain little or no glucose, she seeks medical attention.As a result of a later medical examination, she learns that she has hyperglycemia, hyperkalemia, and a high plasma osmo-lality.When she shows the doctor her EKG that she recorded in the physiology lab, he remarks that it has some abnormalities.

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...

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.

Functions of the Adrenal Medulla

Produces an effect similar to continuous sympathetic nerve stimulation. The symptoms of this condition are hypertension, elevated metabolism, hyperglycemia and sugar in the urine, nervousness, digestive problems, and sweating. It does not take long for the body to become totally fatigued under these conditions, making the patient susceptible to other diseases.

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...

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 P-cell function through regenerating P-cells from islet cell precursors is an attractive alternative to transplantation of exogenous P-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,...

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 .

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.

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...

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., 1990). 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.

Pathophysiology of the Metabolic Syndrome

Increased circulating FFA has been hypothesized to lead to tissue-specific lipotoxicity (Kusminski et al, 2009 Unger, 2003). Elevated FFA levels inhibit insulin-stimulated skeletal muscle glucose uptake and increase hepatic glucose production (Boden, 1999), thus contributing to peripheral insulin resistance. Further, the increase in FFA levels promotes increased hepatic triglyceride synthesis and storage, and the excess triglycerides are secreted as very low-density lipoproteins (VLDL) (Lewis, 1997), which lead to an increased production of LDL. Elevated plasma triglycerides are inversely correlated with HDL-C levels (Austin, 1989), which is thought to occur by the action of cholesteryl ester transfer protein (Sandhofer et al, 2006). This leads to smaller, triglyceride-rich HDL particles with higher catabolic rate due to increased renal clearance, which results in reduced HDL levels (Ji et al, 2006). In similar fashion, elevated triglyceride levels lead to formation of atherogenic...

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...

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

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...

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.

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

Diabetes Mellitus and Hypoglycemia

Inadequate secretion of insulin, or defects in the action of insulin, produce metabolic disturbances that are characteristic of diabetes mellitus. A person with type 1 diabetes requires injections of insulin a person with type 2 diabetes can control this condition by other methods. In both types, hyperglycemia and glycosuria result from a deficiency and or inadequate action of insulin. A person with reactive hypoglycemia, by contrast, secretes excessive amounts of insulin and thus experiences hypoglycemia in response to the stimulus of a carbohydrate meal. Chronic high blood glucose, or hyperglycemia, is the hallmark of diabetes mellitus. The name of this disease is derived from the fact that glucose spills over into the urine when the blood glucose concentration is too high (mellitus is derived from a Latin word meaning honeyed or sweet). The general term diabetes comes from a Greek word meaning siphon it refers to the frequent urination associated with this condition. The...

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).

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...

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...

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

Defining Adherence

Hypertensive treatment may create a rise in various serum cholesterol measures by 4-56 however, Ott and colleagues (2003) conducted an RCT in elderly that did not find such differences (Ott et al, 2003). Similarly, anti-hyperglycemic agents may lower blood glucose levels and gly-cated hemogloblin (HbA1c), but may lead to an increase in serum cholesterol (Gershberg et al, 1968). Thus, attempts to establish an optimal adherence to a cholesterol lowering regimen may potentially be confounded by adherence to the concurrent hypertension or diabetes regimen.

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


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


Rosemary, a 32-year-old office worker, discovers after taking a physical that she has hypertension and hyperglycemia. She returns to take an oral glucose tolerance test, which is found to be normal. Blood tests reveal normal blood levels of T4 and T3, but more extensive tests show that her blood cortisol levels are abnormally high. Rosemary has a generalized puffiness, but not myxedema. Upon questioning, she states that she does not have a history of chronic inflammation and has not been taking immunosuppressive drugs.

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,...


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).

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...

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,...

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.

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

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...

Agerelated cataract

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...

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