Angiotensin II receptor blockers decreased blood glucose levels: a longitudinal survey using data from electronic medical records

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Abstract

Background

A beneficial effect on glucose metabolism is reported with angiotensin receptor blocker (ARB) treatment of hypertension. The effect on blood glucose level during the course of treatment with ARBs in clinical cases is uncertain. Our objectives were to survey the changes in glucose and HbA1c levels in patients with hypertension over a one-year period, and to study the correlations between these values and the time after the start of ARB therapy.

Methods

We conducted a retrospective longitudinal survey of blood glucose and HbA1c measurements in Japanese patients aged ≥20 years with newly diagnosed hypertension but without diabetes, who had received ARB monotherapy with candesartan cilexetil, losartan potassium, olmesartan medoxomil, telmisartan, or valsartan during the period from December 2004 to November 2005. Data including 2465 measurements of non-fasting blood glucose in 485 patients and 457 measurements of HbA1c in 155 patients were obtained from electronic medical records of Nihon University School of Medicine. Linear mixed effects models were used to analyze the relationship between these longitudinal data of blood examinations and covariates of patient age, sex, medication, and duration of ARB therapy.

Results

Casual blood glucose level was associated with the duration of treatment (P < 0.0001), but not with age, sex, or medication. Blood glucose level was significantly decreased during the periods of 0~3 months (P < 0.0001) and 3~6 months (P = 0.0081) compared with baseline, but was not significantly different between 6~12 months and baseline. There was no association between HbA1c level and covariates of sex, age, medication and duration of treatment.

Conclusion

Our findings provide new clinical evidence that the effects of ARBs on glucose metabolism may change during the course of treatment, suggesting a blood glucose-lowering effect in the short-term after the start of treatment.

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Most cited references 17

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Blockade of the renin-angiotensin system increases adiponectin concentrations in patients with essential hypertension.

H. Murakami, Nobuyuki Ura, Marenao Tanaka … (2003)

Adiponectin, an adipocyte-derived protein, has been suggested to play an important role in insulin sensitivity. We examined the association between insulin sensitivity (M value) evaluated by the euglycemic-hyperinsulinemic glucose clamp and adiponectin concentrations in 30 essential hypertensives (EHT) and 20 normotensives (NT) and investigated the effect of blockade of the renin-angiotensin system (RAS) on adiponectin concentrations. EHT were divided into 12 insulin-resistant EHT (EHT-R) and 18 non-insulin-resistant EHT (EHT-N) using mean-1 SD of the M value in NT. There were no intergroup differences in age, gender, and body mass index (BMI). EHT-R had significantly higher levels of insulin and triglyceride and lower levels of adiponectin than did NT and EHT-N. EHT-R had higher levels of free fatty acid and lower levels of high-density lipoprotein (HDL) cholesterol than did EHT-N. Adiponectin concentrations were positively correlated with M value and HDL cholesterol and negatively correlated with BMI, insulin, free fatty acid, and triglyceride but not with blood pressure. M value, BMI, and HDL cholesterol were independent determinants of adiponectin concentrations in multiple and stepwise regression analyses. Sixteen EHT were treated with an angiotensin-converting enzyme inhibitor (temocapril, 4 mg/d; n=9) or an angiotensin II receptor blocker (candesartan, 8 mg/d; n=7) for 2 weeks. Treatment with temocapril or candesartan significantly decreased blood pressure and increased M value and adiponectin concentrations but did not affect BMI and HDL cholesterol. These results suggest that hypoadiponectinemia is related to insulin resistance in essential hypertension and that RAS blockade increases adiponectin concentrations with improvement in insulin sensitivity.

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Report of the Committee on the classification and diagnostic criteria of diabetes mellitus

Takeshi Kuzuya, Shoichi Nakagawa, Jo Satoh … (2002)

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Insulin-mediated sympathetic stimulation: role in the pathogenesis of obesity-related hypertension (or, how insulin affects blood pressure, and why).

L Landsberg (2001)

Thus, the evidence summarized here supports an important role for insulin and the sympathetic nervous system in the pathogenesis of obesity-related hypertension. Is it possible that insulin-mediated sympathetic stimulation contributes a pro-hypertensive effect in non-obese as well? It seems possible in young borderline hypertensives where sympathetically mediated thermogenic mechanisms are potent enough to compensate for the increased caloric intake, thereby enabling these young hypertensives to avoid obesity. This is consistent with an observation made in the original Framingham cohort that not only did obesity predict the eventual development of hypertension, but hypertension, as well, predicted the eventual development of obesity. A reasonable interpretation of these data suggests that as subjects age and the effectiveness of thermogenic mechanisms wanes, obesity might develop as a consequence of increased caloric intake no longer effectively buffered by the increased SNS activity. It is important to note that the mechanisms described here exert a pro-hypertensive effect and cannot properly be considered to 'cause' hypertension. Hypertension is rarely the consequence of a single mechanism. It is also true, as pointed out convincingly by Julius and his colleagues, that enhanced sympathetic activity, as a primary factor, can be associated with both hypertension, insulin resistance and, possibly, obesity [39]. And, finally, it should be noted that the mechanism described here is not the only mechanism linking obesity and hypertension. A rapidly emerging body of evidence indicates that leptin, the polypeptide product of the ob/ob gene secreted from adipose tissue, exerts potent central neural effects on both appetite and sympathetic activity. Leptin levels, elevated in obese humans, have the potential to increase both sympathetic activity and blood pressure [40-43]. A more comprehensive summary of the relationships between hypertension and obesity may, therefore, involve insulin and leptin, as well as the SNS, as represented in the schema presented in Figure 7. Both leptin and insulin may, therefore, be considered as compensatory mechanisms recruited to restore energy balance, with the SNS as one of the effector arms. Viewed in this way, obesity-related hypertension is inextricably linked to the metabolic economy of the obese.

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Author and article information

Journal

Journal ID (nlm-ta): Cardiovasc Diabetol

Title: Cardiovascular Diabetology

Publisher: BioMed Central

ISSN (Electronic): 1475-2840

Publication date Collection: 2007

Publication date (Electronic): 29 September 2007

Volume: 6

Page: 26

Affiliations

[1 ]Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan

[2 ]Division of Genomic Epidemiology and Clinical Trials, Advanced Medical Research Center, Nihon University School of Medicine, Tokyo, Japan

[3 ]Clinical Laboratory, Nihon University Nerima-Hikarigaoka Hospital, Tokyo, Japan

Article

Publisher ID: 1475-2840-6-26

DOI: 10.1186/1475-2840-6-26

PMC ID: 2098751

PubMed ID: 17903269

SO-VID: 204315c0-a190-4845-bd01-a50ca3073c10

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Angiotensin II receptor blockers decreased blood glucose levels: a longitudinal survey using data from electronic medical records

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Abstract

Background

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Most cited references 17

Blockade of the renin-angiotensin system increases adiponectin concentrations in patients with essential hypertension.

Report of the Committee on the classification and diagnostic criteria of diabetes mellitus

Insulin-mediated sympathetic stimulation: role in the pathogenesis of obesity-related hypertension (or, how insulin affects blood pressure, and why).

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