The contribution of skeletal muscle tumor necrosis factor-α to insulin resistance and hypertension in fructose-fed rats

Togashi, Nobuhiko; Ura, Nobuyuki; Higashiura, Katsuhiro; Murakami, Hideyuki; Shimamoto, Kazuaki

doi:10.1097/00004872-200018110-00011

Cited by 93 publications

(91 citation statements)

References 35 publications

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“…[8][9][10][11][12][13][14]16 However, how the upregulation of these proteins decays after the withdrawal of RAS activation has remained unclear.…”

Section: Discussionmentioning

confidence: 99%

“…12 Briefly, on the day before the GC experiments, the rats were anesthetized, and the right common carotid artery and the right jugular vein were cannulated with polyethylene tubes (PE50; Becton Dickinson and Co., Sparks, MD, USA) for collecting blood samples and administration of the infusion. After overnight fasting (approximately 12 h), each conscious rat was placed in a foam plastic jacket.…”

Section: Euglycemic Hyperinsulinemic Gc Techniquementioning

confidence: 99%

“…The tissue level of tumor necrosis factor-a (TNF-a) was determined as previously reported. 12 Briefly, the muscle tissues were homogenized with a polytron homogenizer (Kinematica, Luzern, Switzerland) in icecold lysis buffer. The resulting solution was centrifuged at 17 500 g for 30 min and the supernatant was assayed for TNF-a, using ELISA kits (Invitrogen Corporation, Carlsbad, CA, USA).…”

Section: Determinations Of Tissue Levels Of Tnf-a Mcp-1 and Tbarsmentioning

confidence: 99%

“…Activation of the AT 1 receptor has been shown to activate multiple signaling pathways, leading to inflammatory reactions in blood vessels, 8,9 adipose tissue 10,11 and skeletal muscles. 12,13 Second, inflammatory reactions are often self-perpetuating 14 and are maintained even after the initial stimuli are withdrawn. Third, inflammatory cytokines and reactive oxygen species (ROS) have been shown to contribute to insulin resistance, 12,[15][16][17][18] which is closely related to the development of hypertension.…”

Section: Introductionmentioning

confidence: 99%

“…12,13 Second, inflammatory reactions are often self-perpetuating 14 and are maintained even after the initial stimuli are withdrawn. Third, inflammatory cytokines and reactive oxygen species (ROS) have been shown to contribute to insulin resistance, 12,[15][16][17][18] which is closely related to the development of hypertension. To test our hypothesis, we examined changes in blood pressure, insulin sensitivity and tissue levels of inflammatory cytokines and ROS production at 4 weeks after a 4-week infusion of Ang II in rats.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II receptor activation in youth triggers persistent insulin resistance and hypertension—a legacy effect?

et al. 2011

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Although the involvement of angiotensin II (Ang II) in insulin resistance and hypertension has been established, the temporal relationships between Ang II receptor activation and changes in insulin sensitivity and blood pressure are not clear. To better understand this issue, we infused rats with Ang II (200 ng kg À1 min À1 ) or vehicle for 4 weeks and assessed the residual effects after the discontinuation of the infusion on blood pressure, insulin sensitivity and tissue parameters of inflammation. Four weeks after the discontinuation of the Ang II infusion, the blood pressure was higher by 12.8 mm Hg, and insulin sensitivity as determined by a euglycemic hyperinsulinemic glucose clamp was reduced (glucose infusion rate: 11.1 ± 0.7 vs. 17.6±0.5 mg kg À1 min À1 ) in the Ang II-treated group compared with controls. The persistent hypertension and insulin resistance were associated with greater than two-fold increases in macrophage chemoattractant protein-1, tumor necrosis factor-a and thiobarbituric acid-reactive substrates in the soleus muscle. Furthermore, total and activated forms of Rac-1, a regulatory subunit of the NADPH oxidase complex, were increased by 144 ± 14% and 277 ± 82%, respectively, in the skeletal muscle of Ang II-treated rats. These residual effects after Ang II infusion were all attenuated by the co-administration of tempol, a free radical scavenger, or candesartan with Ang II. The effects of candesartan were not mimicked by hydralazine at an equidepressant dose. These findings suggest that Ang II receptor activation in youth triggers the upregulation of inflammatory cytokines and the production of reactive oxygen species, thereby inducing later insulin resistance and hypertension. INTRODUCTIONEvidence from patients and animal models has indicated that the angiotensin II (Ang II) type 1 receptor (AT 1 receptor) has a major role in the development of insulin resistance and hypertension. 1-4 However, the relationship between timing of the AT 1 receptor activation and the development (and persistence) of changes in insulin sensitivity and blood pressure has not been fully elucidated. Interestingly, the Trial of Preventing Hypertension Study showed that the treatment of prehypertensive patients with the AT 1 receptor blocker (ARB) candesartan for 2 years significantly delayed the progression from pre-hypertension to stage 1 hypertension during the following 2 years. 5 This finding suggests long-lasting effects of transitory activation of the AT 1 receptor in the development of hypertension. The results of the Trial of Preventing Hypertension Study bear certain similarities to those of a study by Holman et al. 6 (United Kingdom Prospective Diabetes Study), indicating the so-called 'legacy effect' . These authors found that the reduction of microvascular events continued for 10 years, in spite of the loss of differences in glycemic control after 10 years of intensive glycemic control had been discontinued. Furthermore, such 'legacy

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“…[8][9][10][11][12][13][14]16 However, how the upregulation of these proteins decays after the withdrawal of RAS activation has remained unclear.…”

Section: Discussionmentioning

confidence: 99%

Section: Euglycemic Hyperinsulinemic Gc Techniquementioning

confidence: 99%

Section: Determinations Of Tissue Levels Of Tnf-a Mcp-1 and Tbarsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Angiotensin II receptor activation in youth triggers persistent insulin resistance and hypertension—a legacy effect?

et al. 2011

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Skeletal Muscle and Exercise

Levine¹,

Levine²

2012

Metabolic Syndrome and Cardiovascular Disease

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Effects of angiotensin receptor‐neprilysin inhibitor on insulin resistance in patients with heart failure

et al. 2023

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Aims Although the haemodynamic effects of angiotensin receptor‐neprilysin inhibitor (ARNI) on patients with heart failure have been demonstrated, the effect on glucose metabolism has not been fully elucidated. We retrospectively investigated the effect of ARNI on abnormal glucose metabolism in patients with stable chronic heart failure using an additional structural equation model (SEM) analysis. Methods We analysed 34 patients who regularly visited to the outpatient department of our institute with heart failure from October 2021 and July 2022 and who were taking angiotensin‐converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). Seventeen patients switched from ACE inhibitors or ARBs to an ARNI (ARNI group), and the other 17 patients continued treatment with ACE inhibitors or ARBs (control group). Results At baseline, although the ARNI group included fewer patients with heart failure with preserved ejection fraction in comparison with the control group (P = 0.004), patients with heart failure with mildly reduced ejection fraction, and heart failure with reduced ejection fraction were mostly biased towards the ARNI group (although not statistically significant). The baseline insulin resistance in the ARNI group was already significantly higher in comparison with the control group [fasting blood insulin, 9.7 (7.4, 11.6) vs. 7.8 (5.2, 9.2) μU/mL, P = 0.033; homoeostasis model assessment of insulin resistance (HOMA‐IR), 3.10 (1.95, 4.19) vs. 2.02 (1.56, 2.42), P = 0.014]. Three months later, the fasting blood insulin and the HOMA‐IR levels were both found to have decreased in comparison with the baseline values [baseline to 3 months: insulin, 9.7 (7.4, 11.6) to 7.3 (4.6, 9.4) μU/mL, P < 0.001; HOMA‐IR, 3.10 (1.95, 4.19) to 1.96 (1.23, 3.09), P < 0.001]. An additional SEM analysis demonstrated that the initiation of ARNI had caused a reduction in the fasting blood insulin and the HOMA‐IR levels at 3 months independently of the baseline fasting blood insulin and HOMA‐IR levels, respectively. Similarly, the initiation of ARNI resulted in a significant reduction in serum uric acid levels (6.28 ± 0.35 to 5.80 ± 0.30 mg/dL, P = 0.008). Conclusions In conclusion, even in a short period of only 3 months, the administration of ARNI improved insulin resistance and consequently reduced the serum uric acid levels in patients with stable chronic heart failure. Although the ARNI group already had high insulin resistance at baseline, an additional SEM analysis revealed that the decreased insulin resistance was truly due to the effect of ARNI.

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The contribution of skeletal muscle tumor necrosis factor-α to insulin resistance and hypertension in fructose-fed rats

Cited by 93 publications

References 35 publications

Angiotensin II receptor activation in youth triggers persistent insulin resistance and hypertension—a legacy effect?

Angiotensin II receptor activation in youth triggers persistent insulin resistance and hypertension—a legacy effect?

Skeletal Muscle and Exercise

Effects of angiotensin receptor‐neprilysin inhibitor on insulin resistance in patients with heart failure

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