UMLS:C0028754 - FACTA Search

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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

5174 Japanese male workers were studied cross-sectionally to examine a possible relationship between obesity and the prevalence of proteinuria (1 + or greater), determined using a reagent strip. The subjects were divided into three groups with body-mass indexes (BMIs) of < 23, 23-24.9 and > or = 25, and the prevalence of proteinuria was compared among the three groups, after adjustments for age, blood pressure and blood levels of HbA1c. Among subjects with hypertension and/or a high level of HbA1c, i.e., > or = 5.9%, the group with a BMI of > or = 25 had a higher prevalence of proteinuria than the group with a BMI of < 23. In contrast, the prevalence of proteinuria was not affected by obesity in the subjects with neither hypertension nor a high level of HbA1c. These results suggest that for obese men with hypertension or diabetes, reducing body weight is important not only as part of the treatment for those diseases, but also to prevent proteinuria.
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PMID:[Relationship between the prevalence of proteinuria and obesity in Japanese men]. 1022 94

We have recently reported that dietary fish oil supplementation (n-3) polyunsaturated fatty acid (PUFA) led to a reduction in blood pressure (BP) and serum triglycerides (TG), in addition to the normalization of the hypercoagulable state in subjects with obesity, hypertension and dyslipidemia without diabetes mellitus (OHD-DM). The aim of the present study was to explore the mechanism of this amelioration by comparing the previous results to those obtained from 19 subjects who, in addition to the conditions described above, also suffer from diabetes mellitus (OHD+DM) and proteinuria. In both the non-diabetic and diabetic groups, a similar reduction was observed in BP (from 158.7/80.8 to 146/72.9 mmHg, and from 157.6/83.2 to 141.9/75.6 mmHg, respectively, P<0.001) and TG levels (from 159.2 to 108.0 mg/dl and from 208.7 to 153.1 mg/dl, respectively, P<0.001). However, a favorable reduction in hemostasis parameters (platelet aggregation on extracellular matrix and (alpha2-antiplasmin) was only seen among the nondiabetic patients (from 12.1+/-4.9 to 4.2+/-3.2%, P<0.001). This difference may stem from a less efficient exchange between n-3 and n-6 PUFA in serum phospholipid of the OHD+DM patients. Overall, this 13-day fasting/refeeding method developed by us has proven to cause the rapid exchange of arachidonic acid for eicosapentaenoic acid. It appears to be an effective regimen for the reduction of cardiovascular risk factors (BP, TG and hemostatic variables) in OHD-DM patients and to a lesser extent in OHD+DM patients.
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PMID:The effect of fish oil on hypertension, plasma lipids and hemostasis in hypertensive, obese, dyslipidemic patients with and without diabetes mellitus. 1050 62

The SHROB rat is a unique strain with genetic obesity, hypertriglyceridemia, hyperinsulinemia, renal disease with proteinuria, and genetically determined hypertension, characteristics paralleling human Syndrome X. The obese phenotype results from a single homozygous recessive trait, designated faK, and is allelic with the Zucker fatty trait (fa), but of distinct origin. The faK mutation is a premature stop codon in the extracellular domain of the leptin receptor, resulting in a natural receptor knockout. The SHROB are glucose intolerant compared to heterozygous or wild-type SHR, but retain fasting euglycemia even on a high sucrose diet, suggesting that diabetes requires polygenic interaction with additional modifier genes. Insulin-stimulated phosphorylation of tyrosine residues on the insulin receptor and on the associated docking protein IRS-1 are reduced in skeletal muscle and liver compared to SHR, due mainly to diminished expression of insulin receptor and IRS-1 proteins. Despite multiple metabolic derangements and severe insulin resistance, hypertension is not exacerbated in SHROB compared to SHR. Thus, insulin resistance and hypertension are independent in this model. Increased activity of the sympathetic nervous system may be a common factor leading by separate pathways to hypertension and to insulin resistance. We studied the chronic effects of sympathetic inhibition with moxonidine on glucose metabolism in SHROB. Moxonidine (8 mg/kg/day), a selective I1-imidazoline receptor agonist, not only reduced blood pressure but also ameliorated glucose intolerance. Moxonidine reduced fasting insulin by 47% and plasma free fatty acids by 30%. Moxonidine enhanced expression and insulin-stimulated phosphorylation of IRS-1 in skeletal muscle by 74 and 27%, respectively. Thus, central sympatholytic therapy not only counters hypertension but also insulin resistance, glucose tolerance, and hyperlipidemia in the SHROB model of Syndrome X.
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PMID:Molecular pathology in the obese spontaneous hypertensive Koletsky rat: a model of syndrome X. 1084 68

Morphologic changes in massive obesity in both humans and experiment animals are rather limited. Glomerulomegaly is common and often asymptomatic. Frequently, ensuing focal and segmental glomerulosclerosis may well be related to alterations in intraglomerular hemodynamics and may result in heavy proteinuria. Factors for the occurrence of segmental glomerulosclerosis have been assessed in animal models and include the influence of lipids. A consequence of surgical therapy for obesity (ie, jejunoileal bypass) is oxalosis with chronic interstitial nephritis, and this may necessitate a takedown of the bypass.
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PMID:Pathology of renal complications in obesity. 1098 Oct 55

Although it is known that renal injury develops in obesity and diabetes mellitus, there have been no investigations examining the impact of insulin resistance per se on the development of renal injury. The present study was undertaken to examine whether insulin resistance and obesity influence urinary protein excretion (UPE) in female heminephrectomized Wistar fatty rats (WFRs). After 24 weeks of heminephrectomy in WFRs, the body weight ([BW], 465+/-18 g; n = 6), blood pressure (155+/-5 mm Hg), serum insulin to glucose ratio (1.31+/-0.39 microU/mg), and daily UPE (24+/-7 mg/d) were greater versus Wistar lean rats ([WLRs] 258+/-8 g, 134+/-1 mm Hg, 0.19+/-0.06 microU/mg, and 5+/-1 mg/d, respectively; n = 6), whereas blood glucose levels did not increase significantly. In WFRs, long-term (ie, 24 weeks) treatment with troglitazone, an insulin-sensitizing agent, improved the serum insulin to glucose ratio (0.17+/-0.09 microU/mg), reduced blood pressure (to 140+/-4 mm Hg), and decreased UPE (to 7+/-1 mg/d), although it had no effect on BW. Of note, with troglitazone treatment, the reduction in proteinuria preceded the correction of hypertension (ie, at week 12). In conclusion, our study suggests that insulin resistance per se causes proteinuria that does not appear to depend on blood pressure. Furthermore, long-term therapy with troglitazone may be a useful tool for the treatment of renal injury in the insulin-resistant condition.
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PMID:Renal protective effect of troglitazone in Wistar fatty rats. 1107 30

The aim of the current study was to characterize the effects of prolonged hyperglycemia on renal structure and function using a model of non-insulin-dependent diabetes mellitus: the Goto Kakizaki (GK) rat, which does not have confounding variables, such as hyperlipidemia, obesity, or elevated blood pressure. The data show that hyperglycemia in this model was not associated with the development of significant proteinuria, but it was associated with the development of definitive age-dependent renal structural changes. These changes consisted of thickening of glomerular basement membrane at 35 weeks and tubular basement membrane. This thickening was accompanied by marked glomerular hypertrophy resulting from a parallel increase in total capillary luminal volume and mesangial volume, but fractional capillary and mesangial volumes remained unchanged. There was evidence of podocyte injury, as assessed by de novo expression of desmin. In contrast, there was no evidence of mesangial cell activation, as assessed by their de novo expression of alpha-SMA. Interstitial monocyte/macrophage influx increased significantly in GK rats at 12 weeks compared with Wistar controls. Glomerular macrophage infiltration was elevated significantly in 35-week GK rats. The structural changes described in the GK rat are similar to those described in prolonged non-insulin-dependent diabetes mellitus patients who have not developed overt renal disease. This model allows us to investigate further the mechanisms involved in the pathogenesis of the consequences of prolonged hyperglycemia.
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PMID:Association of prolonged hyperglycemia with glomerular hypertrophy and renal basement membrane thickening in the Goto Kakizaki model of non-insulin-dependent diabetes mellitus. 1115 83

Diabetic nephropathy is the most common single cause of end-stage renal failure (ESRF) in the Western world, recorded as the cause of renal failure in up to 40% to 45% of those entering renal replacement therapy (RRT) programs. However, marked differences exist between countries; the percentage of patients entering RRT in Norway because of diabetic nephropathy is 10% of the incident RRT population. The percentage in the United States is approximately 40%; therefore, the purpose of the present study was to compare data from Norway with data from the United States in an attempt to detect factors that might explain some of the differences. To make the comparisons as valid as possible, an attempt has been made to focus on populations of similar genetic make-up. The incidence of type 1 diabetes is a little higher in Norway than in the United States, whereas the prevalence of type 2 diabetes may be twice as high in the United States as in Norway; marked differences in the prevalence of obesity is probably a significant causative factor. There seems to be no striking difference in the prevalence of microalbuminuria in people with diabetes in the two populations, whereas there are insufficient data to compare the prevalence of overt proteinuria. The incidence of patients with a diagnosis of diabetic nephropathy as the cause of ESRF entering RRT in the two study populations showed marked differences; the incidence for 1997 was 8.9/million population in Norway and 113/million population in the United States. The proportion of type 2 diabetes was 46% in Norway and 64% in the US (1997). It is unlikely that the marked difference in incidence of RRT can be explained by differences in type 2 diabetes prevalence alone. The populations may not be directly comparable, and differences in the size of study populations and in the choice of renal diagnosis in patients with diabetes as a comorbid factor at the beginning of RRT may introduce uncertainties. Further, data on other factors--such as incidence of death before RRT is indicated, quality of care, and health care delivery, expressed as degree of blood pressure and metabolic control--were not available. Differences in acceptance of diabetes patients into RRT programs are not believed to contribute significantly. Norway is seeing a development toward increasing body weight and a change toward a more sedentary lifestyle, together with an increasing prevalence of type 2 diabetes earlier in life than has previously been the case. An increase in diabetic nephropathy and need for RRT because of type 2 diabetes must therefore be expected in Norway. To understand differences and to best design preventive programs, further comparative studies of the two populations seem warranted.
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PMID:Diabetic nephropathy and end-stage renal failure: the Norwegian story. 1117 23

Experimental evidence suggests a role for obesity in the formation and progression of some glomerular lesions, but data for human glomerulonephritis are lacking. In a cohort of 162 incident patients with biopsy-proven immunoglobulin A (IgA) nephropathy, we assessed whether the presence of an elevated body mass index (BMI >/= 25 kg/m(2)) at the time of the first renal biopsy (RB1) correlated with clinical data at RB1 (24-hour proteinuria, arterial hypertension, and renal function), pathological data (global optical score [GOS] with detailed pathological indices), and clinical progression to both arterial hypertension and chronic renal failure (CRF). In both univariate and multivariate analyses, the presence of an elevated BMI at RB1 was significantly associated with the severity of pathological renal lesions (GOS and vascular, tubular, and interstitial indices). Hypertension-free survival was significantly less in overweight patients (P: < 0.0001) compared with those with normal weight. In a Cox regression analysis for hypertension-free survival including 24-hour proteinuria greater than 1 g, GOS, and metabolic parameters, only elevated BMI and GOS were independent factors for the development of arterial hypertension. CRF-free survival was also significantly less in patients with an excessive BMI. In a multivariate Cox regression analysis for CRF-free survival, hypertension, GOS, and BMI at RB1 were independent risk factors for CRF. In IgA nephropathy, excessive body weight and/or BMI are underestimated predictive factors for the development of arterial hypertension and, ultimately, CRF.
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PMID:Excessive body weight as a new independent risk factor for clinical and pathological progression in primary IgA nephritis. 1127 71

Wistar fatty (WF) rats have a genetic predisposition to hyperglycemia, polyuria, hyperinsulinemia, hyperlipidemia, obesity and nephropathy. These phenotypic characteristics are similar to those observed in obese patients with non-insulin-dependent diabetes mellitus (NIDDM) nephropathy. In this study, the effects of two types of renin-angiotensin system inhibitors, an angiotensin II type 1-receptor antagonist (AT1A) and an angiotensin I-converting enzyme inhibitor (ACEI), on renal injury in WF rats were studied during the progressive phase of diabetic nephropathy. An AT1A, candesartan cilexetil (1 mg/kg), and an ACEI, enalapril (10 mg/kg), were administered orally once a day for 12 weeks, beginning when the rats were 27-week-old and already showed diabetic nephropathy and obesity. Both drugs prevented an increase in proteinuria during the experimental period. Furthermore, after 4-week intervention, the levels of proteinuria were markedly lower in drug-treated rats. At the end of the experiment, both drugs prevented the development of glomerular lesions without affecting glucose metabolism and obesity. In conclusion, the inhibition of angiotensin II activity ameliorated both existing proteinuria and the progression of proteinuria, resulting in preservation of glomerular structure. Thus angiotensin II plays important roles in the development and the progression of nephropathy in genetically obese diabetic WF rats.
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PMID:Involvement of angiotensin II in progression of renal injury in rats with genetic non-insulin-dependent diabetes mellitus (Wistar fatty rats). 1138 46

Atherosclerosis and coronary artery disease (CAD) are now the commonest sequelae of hypertension and all clinical manifestations of CAD occur in excess in persons with elevated blood pressure. Risk increases in relation to the extent of blood pressure elevation whether this is in the systolic or diastolic component, at any age and in either sex. Even isolated systolic hypertension increases cardiovascular risk. Elevated pressures are often accompanied by lipid abnormalities, hyperglycemia, elevated fibrinogen, obesity, and ECG abnormalities, all of which augment the risk. These risk factors associated with hypertension influence the coronary risk potential more than the nature of the blood pressure elevation. Although blood pressure makes an independent contribution to CAD, the risk at any level of pressure is markedly influenced by the cardiovascular risk profile. In mild to moderate hypertension in particular, the risk of CHD is concentrated in those who have impaired glucose tolerance, increased total/HDL ratio, ECG abnormalities, and smoke cigarettes. One or more of these associated risk factors also predisposes to other cardiovascular sequelae of hypertension, including stroke, peripheral vascular disease, and cardiac failure. The presence of organ involvement indicated by proteinuria, evidence of impaired ventricular function, or left ventricular hypertrophy greatly escalates the risk and usually indicates a compromised coronary circulation. Most myocardial infarctions and sudden deaths occur prior to the appearance of such evidence. Hypertensive risk assessment requires consideration of the multivariate risk profile because of the interdependence of the risk factors. The nature and urgency of treatment is better determined from such a risk profile than from the blood pressure parameters alone. Optimal preventive management of hypertension requires more than normalization of the blood pressure if coronary sequelae are to be avoided.
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PMID:Influence of multiple risk factors on the hazard of hypertension. 1152 37

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