Impact of age, body mass index, insulin resistance and proteinuria on the kidney function in obese patients with Type 2 diabetes and renal insufficiency

2008 ◽  
Vol 69 (01) ◽  
pp. 10-17 ◽  
Author(s):  
M. Koch ◽  
A. Beien ◽  
A. Fusshöller ◽  
S. Zitta ◽  
B. Haastert ◽  
...  
2010 ◽  
Vol 63 (9-10) ◽  
pp. 611-615 ◽  
Author(s):  
Branka Koprivica ◽  
Teodora Beljic-Zivkovic ◽  
Tatjana Ille

Introduction. Insulin resistance is a well-known leading factor in the development of metabolic syndrome. The aim of this study was to evaluate metabolic effects of metformin added to sulfonylurea in unsuccessfully treated type 2 diabetic patients with metabolic syndrome. Material and methods. A group of thirty subjects, with type 2 diabetes, secondary sulfonylurea failure and metabolic syndrome were administered the combined therapy of sulfonylurea plus metformin for six months. Metformin 2000 mg/d was added to previously used sulfonylurea agent in maximum daily dose. Antihypertensive and hypolipemic therapy was not changed. The following parameters were assessed at the beginning and after six months of therapy: glycemic control, body mass index, waist circumference, blood pressure, triglycerides, total cholesterol and its fractions, homeostatic models for evaluation of insulin resistance and secretion (HOMA R, HOMA B) and C- peptide. Results. Glycemic control was significantly improved after six months of the combined therapy: (fasting 7.89 vs. 10.61 mmol/l. p<0.01; postprandial 11.12 vs. 12.61 mmol/l. p<0.01, p<0.01; glycosylated hemoglobin 6.81 vs. 8.83%. p<0.01). the body mass index and waist circumference were significantly lower (26.7 vs. 27.8 kg/m2, p<0.01 and 99.7 vs. 101.4 cm for men, p<0.01; 87.2 vs. 88.5 for women, p<0.01). Fasting plasma triglycerides decreased from 3.37 to 2.45 mmol/l (p<0.001) and HOMA R from 7.04 to 5.23 (p<0.001). No treatment effects were observed on blood pressure, cholesterol, and residual insulin secretion. Conclusion. Administration of metformin in type 2 diabetes with metabolic syndrome decreased cardiovascular risk factors by reducing glycemia, triglycerides, BMI, central obesity and insulin resistance.


2018 ◽  
Vol 31 (9) ◽  
pp. 478 ◽  
Author(s):  
Ana Margarida Monteiro ◽  
Vera Fernandes ◽  
Cláudia Matta-Coelho ◽  
Sílvia Paredes ◽  
Maria Lopes Pereira ◽  
...  

Introduction: We aim to define the iron deficiency prevalence and eventual differences between obese patients with and without metabolic syndrome.Material and Methods: Analysis of patients evaluated at multidisciplinary consultation of obesity in our institution between 2013 and 2015 (n = 260). Iron deficiency: ferritin levels < 15 ng/mL. Exclusion criteria: prior bariatric surgery; lack of ferritin or hemoglobin determinations.Results: We analyzed data from 215 patients (84.2% female) with a mean age of 42.0 ± 10.3 years. The median body mass index was 42.5 (40.0 - 46.8) kg/m2 and 52.1% had metabolic syndrome. Iron deficiency was present in 7.0%, with no differences between genders or between patients with or without metabolic syndrome. Hypertension was associated with lower prevalence of iron deficiency. Type 2 diabetes and hypertension patients had higher levels of ferritin. The multivariate analysis showed that metabolic syndrome and increasing body mass index were predictive of higher risk of iron deficiency while hypertension predicted lower odds of iron deficiency.Discussion: The prevalence of iron deficiency was similar in other published studies. Iron deficiency may be underdiagnosed if based only on ferritin concentrations. In our study, diabetes and hypertension appear to contribute to the increase in ferritin levels described in obesity.Conclusion: Ferritin may not be a reliable index for evaluating iron stores in obese patients, particularly when associated with comorbidities such as type 2 diabetes and hypertension. Further studies are needed to guide the diagnosis and iron supplementation in these patients.


2017 ◽  
Vol 04 (01) ◽  
pp. e1-e4
Author(s):  
Gottfried Rudofsky ◽  
Tanja Haenni ◽  
John Xu ◽  
Eva Johnsson

Abstract Genital infections are associated with sodium glucose co-transporter 2 inhibitors such as dapagliflozin. Since patients with Type 2 diabetes are at increased risk of genital infections, and obesity is a risk factor for infections, obese patients with Type 2 diabetes could be more susceptible to genital infections when treated with sodium glucose co-transporter 2 inhibitors. This pooled dataset assessed the frequency of genital infections according to baseline body mass index in patients treated with dapagliflozin 10 mg. Data were pooled from 13 studies of up to 24 weeks’ duration (dapagliflozin N=2 360; placebo N=2 295). Frequency of genital infections was compared between three body mass index subgroups (<30, ≥30−< 35 and ≥35 kg/m2). Genital infections were reported in 130 (5.5%) patients receiving dapagliflozin and 14 (0.6%) patients receiving placebo; none of which were serious. Genital infections were more common in women (84/130 [64.6%]) than in men (46/130 [35.4%]) treated with dapagliflozin. In the body mass index < 30, ≥ 30−< 35 and ≥ 35 kg/m2 dapagliflozin-treated subgroups, 38/882 (4.3%), 47/796 (5.9%) and 45/682 (6.6%) patients presented with genital infections, respectively. Although the frequency was low overall and relatively similar between subgroups, there was a trend towards an increase in genital infections in patients with a higher body mass index. This trend is unlikely to be clinically relevant or to affect suitability of dapagliflozin as a treatment option for obese patients with Type 2 diabetes, but rather should influence advice and counselling of overweight patients on prevention and treatment of genital infections.


2021 ◽  
Author(s):  
Beatriz Teresita Martín-Márquez ◽  
Flavio Sandoval-Garcia ◽  
Mónica Vazquez-Del Mercado ◽  
Erika-Aurora Martínez-García ◽  
Fernanda-Isadora Corona-Meraz ◽  
...  

2016 ◽  
Vol 144 (9-10) ◽  
pp. 497-502
Author(s):  
Teodora Beljic-Zivkovic ◽  
Milica Marjanovic-Petkovic ◽  
Miljanka Vuksanovic ◽  
Ivan Soldatovic ◽  
Dobrila Kanlic ◽  
...  

Introduction. A combination of drugs is required for treatment of obese subjects with diabetes, due to multiple pathogenic mechanisms implicated in the development of both diabetes and obesity. Objective. Assessment of the effect of sitagliptin added to insulin glargine and metformin, in obese subjects with type 2 diabetes. Methods. A total of 23 obese subjects on metformin and insulin glargine participated in the study. Titration of insulin glargine during a one-month period preceded the addition of 100 mg of sitagliptin daily. Body mass index, waist circumference, fasting, and prandial glucose were measured monthly, lipids and hemoglobin A1c (HbA1c) every three months, insulin, c-peptide and glucagon at the start and after six months of treatment. Homeostatic models for insulin secretion (HOMA B) and insulin resistance (HOMA IR) were calculated. Results. Participants were 58.65 ?} 7.62 years of age with a body mass index of 35.06 ?} 5.15 kg/m2, waist circumference of 115.04 ?} 15.5 cm, and the duration of diabetes of 4.11 ?} 2.57 years. With the titration of insulin glargine, target fasting glucose levels were not achieved. Waist circumference and body mass index decreased during three months of sitagliptin treatment, thereafter remaining stable. HbA1c decreased significantly after three and six months of therapy. C-peptide increased significantly, while glucagon level fell. HOMA indexes were unchanged. Conclusion. Sitagliptin can improve diabetes control and induce modest weight loss in obese subjects poorly controlled on insulin glargine and metformin. Titration of insulin glargine to optimal fasting glucose values is a prerequisite of success of this combination therapy.


2017 ◽  
Vol 5 (3) ◽  
pp. 316-318 ◽  
Author(s):  
Serdar Olt ◽  
Sabri ÖzdaÅŸ ◽  
Mehmet Åžirik

AIM: To investigate the effect of bariatric surgery on HbA1c and serum cortisol levels in morbidly obese patients without type 2 diabetes mellitus.MATERIALS AND METHODS: Twenty-nine patients who underwent sleeve gastrectomy and whose body mass index was> 40 were included in the present study. Patients' files were reviewed retrospectively. Those with diabetes mellitus and those with age <18 were excluded from the study. Pre-operative and 1-year post operative data were documented. The obtained data were analysed by SPSS statistical program.RESULTS: The mean age of the patients was 27.4 ± 8.4. 5 of the patients were male, and 24 were female. The mean body mass index of the patients was 44 ± 2.3. 1 patient [3.4%] had hypertension. Four patients [13.7%] had gastroesophageal reflux disease. The number of smokers was 7 [24.1%], and the number of alcohol users was 3 [10.3%]. There was a statistically significant decrease in HbA1c, body mass index values after operation [p value <0.01], but cortisol was not different [p value = 0.72].CONCLUSION: In this present study we found that bariatric surgery caused a significant decrease in HbA1c levels in non-diabetic patients, suggesting that bariatric surgery may prevent Type 2 Diabetes Mellitus in obese patients.


2001 ◽  
Vol 86 (11) ◽  
pp. 5450-5456 ◽  
Author(s):  
Lidia Maianu ◽  
Susanna R. Keller ◽  
W. Timothy Garvey

Insulin resistance in type 2 diabetes is due to impaired stimulation of the glucose transport system in muscle and fat. Different defects are operative in these two target tissues because glucose transporter 4 (GLUT 4) expression is normal in muscle but markedly reduced in fat. In muscle, GLUT 4 is redistributed to a dense membrane compartment, and insulin-mediated translocation to plasma membrane (PM) is impaired. Whether similar trafficking defects are operative in human fat is unknown. Therefore, we studied subcellular localization of GLUT4 and insulin-regulated aminopeptidase (IRAP; also referred to as vp165 or gp160), which is a constituent of GLUT4 vesicles and also translocates to PM in response to insulin. Subcutaneous fat was obtained from eight normoglycemic control subjects (body mass index, 29 ± 2 kg/m2) and eight type 2 diabetic patients (body mass index, 30 ± 1 kg/m2; fasting glucose, 14 ± 1 mm). In adipocytes isolated from diabetics, the basal 3-O-methylglucose transport rate was decreased by 50% compared with controls (7.1 ± 2.9 vs. 14.1 ± 3.7 mmol/mm2 surface area/min), and there was no increase in response to maximal insulin (7.9 ± 2.7 vs. 44.5 ± 9.2 in controls). In membrane subfractions from controls, insulin led to a marked increase of IRAP in the PM from 0.103 ± 0.04 to 1.00± 0.33 relative units/mg protein, concomitant with an 18% decrease in low-density microsomes and no change in high-density microsomes (HDM). In type 2 diabetes, IRAP overall expression in adipocytes was similar to that in controls; however, two abnormalities were observed. First, in basal cells, IRAP was redistributed away from low-density microsomes, and more IRAP was recovered in HDM (1.2-fold) and PM (4.4-fold) from diabetics compared with controls. Second, IRAP recruitment to PM by maximal insulin was markedly impaired. GLUT4 was depleted in all membrane subfractions (43–67%) in diabetes, and there was no increase in PM GLUT4 in response to insulin. Type 2 diabetes did not affect the fractionation of marker enzymes. We conclude that in human adipocytes: 1) IRAP is expressed and translocates to PM in response to insulin; 2) GLUT4 depletion involves all membrane subfractions in type 2 diabetes, although cellular levels of IRAP are normal; and 3) in type 2 diabetes, IRAP accumulates in membrane vesicles cofractionating with HDM and PM under basal conditions, and insulin-mediated recruitment to PM is impaired. Therefore, in type 2 diabetes, adipocytes express defects in trafficking of GLUT4/IRAP-containing vesicles similar to those causing insulin resistance in skeletal muscle.


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