Metabolic Factors Associated with Benign Prostatic Hyperplasia

Abstract Context: Benign prostatic hyperplasia poses a significant public health problem, but its etiology remains unclear. Obesity and associated abnormalities in glucose homeostasis may play a role in benign prostatic hyperplasia development by influencing prostate growth. Objective: The objective of this study was to determine whether obesity, fasting plasma glucose concentration, and diabetes are associated with radiologically determined prostate enlargement, an objective measure of benign prostatic hyperplasia. Design: This study was a cross-sectional analysis with robust variance estimates to account for multiple measures over time in the same individuals. Setting: This prospective cohort study was composed of community volunteers. Patients: Patients studied were 422 adult men enrolled in The Baltimore Longitudinal Study of Aging. Main Outcome Measurements: Total prostate volume as determined by pelvic magnetic resonance imaging was measured. Results: Among 422 participants, 91 (21.6%) had prostate enlargement (defined as total prostate volume ≥ 40 cc) at first visit. Compared with men of normal weight [body mass index (BMI) < 25 kg/m2], the age-adjusted odds ratio (OR) for prostate enlargement for overweight men (BMI, 25–29.9 kg/m2) was 1.41 (95% CI, 0.84–2.37), for obese men (BMI, 30–34 kg/m2) was 1.27 (95% CI, 0.68–2.39), and for severely obese men (BMI ≥ 35 kg/m2) was 3.52 (95% CI, 1.45–8.56) (P = 0.01). Men with elevated fasting glucose (>110 mg/dl) were more likely to have an enlarged prostate than men with normal fasting glucose (≤110 mg/dl) (OR, 2.98; 95% CI, 1.70–5.23), as were men with a diagnosis of diabetes (OR, 2.25; 95% CI, 1.23–4.11). Conclusions: Obesity, elevated fasting plasma glucose, and diabetes are risk factors for benign prostatic hyperplasia.

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Effects of changes in obesity and exercise on the development of diabetes and return to normal fasting plasma glucose levels at one-year follow-up in middle-aged subjects with impaired fasting glucose

Environmental Health and Preventive Medicine ◽

10.1007/bf02897959 ◽

2001 ◽

Vol 6 (2) ◽

pp. 127-131 ◽

Cited By ~ 4

Author(s):

Shin'ichi Shimizu ◽

Yuichi Kawata ◽

Norito Kawakami ◽

Hideyasu Aoyama

Keyword(s):

Impaired Fasting Glucose ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Fasting Glucose ◽

Middle Aged ◽

Glucose Levels ◽

Fasting Plasma ◽

Aged Subjects ◽

One Year

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Erratum: Fasting Plasma Glucose and Incidence of Diabetes --- Implication for the Threshold for Impaired Fasting Glucose: Results from the Population-Based Omiya MA Cohort Study[Journal of Atherosclerosis and Thrombosis 1606 857-861]

Journal of Atherosclerosis and Thrombosis ◽

10.5551/jat.erra1 ◽

2010 ◽

Vol 17 (3) ◽

pp. 315-315

Author(s):

Masayuki Kato ◽

Mitsuhiko Noda ◽

Hiroshi Suga ◽

Masahiko Matsumoto ◽

Yasunori Kanazawa

Keyword(s):

Cohort Study ◽

Impaired Fasting Glucose ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Fasting Glucose ◽

Population Based ◽

Fasting Plasma

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Fasting Plasma Glucose and Incidence of Diabetes --- Implication for the Threshold for Impaired Fasting Glucose: Results from the Population-Based Omiya MA Cohort Study

Journal of Atherosclerosis and Thrombosis ◽

10.5551/jat.1792 ◽

2009 ◽

Vol 16 (6) ◽

pp. 857-861 ◽

Cited By ~ 13

Author(s):

Masayuki Kato ◽

Mitsuhiko Noda ◽

Hiroshi Suga ◽

Masahiko Matsumoto ◽

Yasunori Kanazawa

Keyword(s):

Cohort Study ◽

Impaired Fasting Glucose ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Fasting Glucose ◽

Population Based ◽

Fasting Plasma

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Effect of telmisartan on selected adipokines, insulin sensitivity, and substrate utilization during insulin-stimulated conditions in patients with metabolic syndrome and impaired fasting glucose

Acta Endocrinologica ◽

10.1530/eje-10-0436 ◽

2010 ◽

Vol 163 (4) ◽

pp. 573-583 ◽

Cited By ~ 11

Author(s):

Petr Wohl ◽

Eva Krušinová ◽

Martin Hill ◽

Simona Kratochvílová ◽

Kateřina Zídková ◽

...

Keyword(s):

Metabolic Syndrome ◽

Insulin Sensitivity ◽

Impaired Fasting Glucose ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Fasting Glucose ◽

Substrate Utilization ◽

Metabolic Effects ◽

Plasma Adiponectin ◽

Fasting Plasma

ObjectiveTelmisartan improves glucose and lipid metabolism in rodents. This study evaluated the effect of telmisartan on insulin sensitivity, substrate utilization, selected plasma adipokines and their expressions in subcutaneous adipose tissue (SAT) in metabolic syndrome.Design and methodsTwelve patients with impaired fasting glucose completed the double-blind, randomized, crossover trial. Patients received telmisartan (160 mg/day) or placebo for 3 weeks and vice versa with a 2-week washout period. At the end of each period, a hyperinsulinemic euglycemic clamp (HEC) combined with indirect calorimetry was performed. During HEC (0, 30, and 120 min), plasma levels of adipokines were measured and a needle biopsy (0 and 30 min) of SAT was performed.ResultsFasting plasma glucose was lower after telmisartan compared with placebo (P<0.05). There were no differences in insulin sensitivity and substrate utilization. We found no differences in basal plasma adiponectin, resistin and tumour necrosis factor α (TNFα), but an increase was found in basal leptin, after telmisartan treatment. Insulin-stimulated plasma adiponectin (P<0.05), leptin and resistin (P<0.001) were increased, whereas TNFα was decreased (P<0.05) after telmisartan treatment. Expression of resistin, but not adiponectin, TNFα and leptin was increased after telmisartan treatment.ConclusionsDespite the decrease in fasting plasma glucose, telmisartan does not improve insulin sensitivity and substrate utilization. Telmisartan increases plasma leptin as well as insulin-stimulated plasma adiponectin, leptin and resistin, and decreases plasma TNFα during HEC. Changes in plasma adipokines cannot be explained by their expressions in SAT. The changes in plasma adipokines might be involved in the metabolic effects of telmisartan in metabolic syndrome.

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The effect of rectal administration of insulin on the short-term treatment of alloxan-diabetic dogs

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y81-001 ◽

1981 ◽

Vol 59 (1) ◽

pp. 1-6 ◽

Cited By ~ 13

Author(s):

Yoshimitsu Yamasaki ◽

Motoaki Shichiri ◽

Ryuzo Kawamori ◽

Toyohiko Morishima ◽

Nobuyoshi Hakui ◽

...

Keyword(s):

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Subcutaneous Injection ◽

Fasting Glucose ◽

Rectal Administration ◽

Subcutaneous Insulin ◽

Glucose Levels ◽

Fasting Plasma ◽

Urinary Glucose ◽

Diabetic Dogs

Six alloxan-diabetic dogs with fasting plasma glucose levels above 200 mg/100 mL were treated with rectal administration of insulin suppositories twice a day for 6–9 days. The effectiveness was compared with that of subcutaneous insulin injections. In three diabetic dogs with fasting plasma glucose levels below 300 mg/100 mL, both insulin suppository at a dose of 20 U (2.3 U/kg) and subcutaneous insulin at a dose of 0.2 U/kg showed a similar effect in reducing fasting glucose levels and daily urinary glucose amounts. In dogs with higher fasting glucose levels, 0.5 U of subcutaneous insulin/kg is less effective in reducing fasting glucose than 50 U (5.2 U/kg) suppositories, in spite of the same effects on daily urinary glucose output. Postprandial glucose responses were significantly lessened with rectal administration of insulin suppositories. The integrated area of increase in peripheral insulin concentration after subcutaneous injection of 0.2 or 0.5 U insulin/kg was significantly greater than that after rectal administration of an insulin suppository (2.3 or 5.2 U/kg, respectively). These results indicate that diabetes could be controlled by the daily rectal administration of an insulin suppository instead of the conventional subcutaneous injection.

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Insulin sensitivity and glucose tolerance improve in patients with acromegaly converted from depot octreotide to pegvisomant

Acta Endocrinologica ◽

10.1530/eje.0.1490521 ◽

2003 ◽

pp. 521-527 ◽

Cited By ~ 88

Author(s):

WM Drake ◽

SV Rowles ◽

ME Roberts ◽

FK Fode ◽

GM Besser ◽

...

Keyword(s):

Body Composition ◽

Insulin Sensitivity ◽

Glucose Tolerance ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

Fasting Glucose ◽

Model Assessment ◽

Median Dose ◽

Fasting Plasma ◽

Igf I

AIM AND METHOD: Insulin resistance leading, in some cases, to glucose intolerance is an important contributory factor to the cardiovascular morbidity and mortality associated with acromegaly. The aim of this study was to document changes in insulin sensitivity (IS) in a group of seven patients with acromegaly (three male, four female, mean+/-s.d. age 59+/-13 Years) treated initially with a stable dose of depot octreotide (OT; median dose 30 mg four times weekly, range 10-30 mg) for a median of 18 Months (range 16-19 Months) and who were then transferred to treatment with pegvisomant (median dose 15 mg daily, range 10-20 mg) for a median of 8 Months (range 7-9 Months). IS was assessed by homeostatic model assessment (HOMA) using fasting glucose and insulin concentrations and by a short insulin tolerance test (sITT). Body composition was assessed by dual energy X-ray absorptiometry. RESULTS: Mean+/-s.d. serum IGF-I concentrations during therapy with OT and with pegvisomant were not statistically different (283+/-119 ng/ml on OT vs 191+/-39 ng/ml on pegvisomant (P=0.4)). However, mean+/-s.d. fasting plasma glucose fell from 6.2+/-1.0 mmol/l on OT to 5.2+/-0.6 mmol/l on pegvisomant (P=0.017) and was lower on pegvisomant in all seven patients. In four patients, fasting plasma glucose fell from values diagnostic of diabetes mellitus or impaired fasting glucose on OT to within the normal range on pegvisomant. Mean+/-s.d. peripheral IS (by sITT) increased from 139+/-39 micromol/l per min on OT to 169+/-59 micromol/l per min on pegvisomant (P=0.037). Mean+/-s.d. IS (by HOMA %S) was unchanged over the course of the study (149.1+/-43.7% on OT vs 139.9+/-76.6% on pegvisomant, P=0.28). Mean+/-s.d. pancreatic beta-cell secretory function (HOMA %B) improved significantly on pegvisomant compared with OT (49.4+/-19.2% vs 82.4+/-43.5%, P=0.01). No statistically significant change in total fat (P=0.3), % fat (P=0.28) or circulating non-esterified fatty acids (P=0.35) was observed. CONCLUSIONS: IS and glucose tolerance improved in patients converted from OT therapy to pegvisomant, without a change in body composition and even when serum IGF-I concentrations remained equally well controlled. This may be an important factor in the choice of medical therapy for patients with acromegaly.

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