Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves

Ribeiro, Rogério; Lautt, W. Wayne; Légaré, Dallas J.; Macedo, M. Paula

doi:10.1007/s00125-005-1714-6

Cited by 59 publications

(69 citation statements)

References 33 publications

(44 reference statements)

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“…31 Animal models suggest that the hepatic parasympathetic nerve dysfunction causes the development of skeletal muscle insulin resistance, linking with the actions of hepatic insulin sensitizing substance (HISS) released from the liver and of the glucose uptake in the skeletal muscle. 32 The hepatic parasympathetic nerves regulate the HISS function; therefore, the impairment potentially lowers peripheral insulin sensitivity, which is consistent with our findings. This HISS hypothesis also implied that parasympathetic dysfunction precedes insulin resistance in the human body.…”

Section: Discussionsupporting

confidence: 91%

Heart Rate Variability, Insulin Resistance and Insulin Sensitivity in Japanese Adults: The Toon Health Study.

Saito

Maruyama

Nishida

et al. 2015

International Journal of Epidemiology

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Background: Although impaired cardiac autonomic function is associated with an increased risk of type 2 diabetes in Caucasians, evidence in Asian populations with a lower body mass index is limited. Methods: Between 2009-2012, the Toon Health Study recruited 1899 individuals aged 30-79 years who were not taking medication for diabetes. A 75-g oral glucose tolerance test was used to diagnose type 2 diabetes, and fasting and 2-h-postload glucose and insulin concentrations were measured. We assessed the homeostasis model assessment index for insulin resistance (HOMA-IR) and Gutt's insulin sensitivity index (ISI). Pulse was recorded for 5 min, and time-domain heart rate variability (HRV) indices were calculated: the standard deviation of normal-to-normal intervals (SDNN) and the root mean square of successive difference (RMSSD). Power spectral analysis provided frequency domain measures of HRV: high frequency (HF) power, low frequency (LF) power, and the LF:HF ratio. Results: Multivariate-adjusted logistic regression models showed decreased SDNN, RMSSD, and HF, and increased LF:HF ratio were associated significantly with increased HOMA-IR and decreased ISI. When stratified by overweight status, the association of RMSSD, HF, and LF:HF ratio with decreased ISI was also apparent in nonoverweight individuals. The interaction between LF:HF ratio and decreased ISI in overweight individuals was significant, with the odds ratio for decreased ISI in the highest quartile of LF:HF ratio in non-overweight individuals being 2.09 (95% confidence interval, 1.41-3.10). Conclusions: Reduced HRV was associated with insulin resistance and lower insulin sensitivity. Decreased ISI was linked with parasympathetic dysfunction, primarily in non-overweight individuals.

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Section: Discussionsupporting

confidence: 91%

Heart Rate Variability, Insulin Resistance and Insulin Sensitivity in Japanese Adults: The Toon Health Study.

Saito

Maruyama

Nishida

et al. 2015

International Journal of Epidemiology

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“…Animals were randomly separated into groups of SC-and HS-fed rodents. In the HS group (n ϭ 6), the drinking water was supplemented with sucrose (35% wt/vol), as described earlier (26), for 2 wk and ingestion of the chow diet and the drinking water tracked daily in both groups. At 7 PM on day 13, all animals received a loading dose of 99% 2 H2O (3 g/100 g body wt), and the corresponding drinking water was also supplemented with 2 H2O to a 3% final enrichment.…”

Section: Methodsmentioning

confidence: 99%

²H enrichment distribution of hepatic glycogen from²H₂O reveals the contribution of dietary fructose to glycogen synthesis

Delgado

Martins

Carvalho

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Delgado TC, Martins FO, Carvalho F, Gonçalves A, Scott DK, O'Doherty R, Macedo MP, Jones JG.2 H enrichment distribution of hepatic glycogen from 2 H2O reveals the contribution of dietary fructose to glycogen synthesis. Am J Physiol Endocrinol Metab 304: E384 -E391, 2013. First published December 4, 2012; doi:10.1152/ajpendo.00185.2012.-Dietary fructose can benefit or hinder glycemic control, depending on the quantity consumed, and these contrasting effects are reflected by alterations in postprandial hepatic glycogen synthesis. Recently, we showed that 2 H enrichment of glycogen positions 5 and 2 from deuterated water ( 2 H2O) informs direct and indirect pathway contributions to glycogenesis in naturally feeding rats. Inclusion of position 6S 2 H enrichment data allows indirect pathway sources to be further resolved into triose phosphate and Krebs cycle precursors. This analysis was applied to six rats that had fed on standard chow (SC) and six rats that had fed on SC plus 35% sucrose in their drinking water (HS). After 2 wk, hepatic glycogenesis sources during overnight feeding were determined by 2 H2O administration and postmortem analysis of glycogen 2 H enrichment at the conclusion of the dark period. Net overnight hepatic glycogenesis was similar between SC and HS rodents. Whereas direct pathway contributions were similar (403 Ϯ 71 mol/g dry wt HS vs. 578 Ϯ 76 mol/g dry wt SC), triose phosphate contributions were significantly higher for HS compared with SC (382 Ϯ 61 vs. 87 Ϯ 24 mol/g dry wt, P Ͻ 0.01) and Krebs cycle inputs lower for HS compared with SC (110 Ϯ 9 vs. 197 Ϯ 32 mol/g dry wt, P Ͻ 0.05). Analysis of plasma glucose 2 H enrichments at the end of the feeding period also revealed a significantly higher fractional contribution of triose phosphate to plasma glucose levels in HS vs. SC. Hence, the 2 H enrichment distributions of hepatic glycogen and glucose from 2 H2O inform the contribution of dietary fructose to hepatic glycogen and glucose synthesis. deuterated water; direct and indirect pathways; fructose; hepatic glycogen; sucrose DIETARY FRUCTOSE CAN SIGNIFICANTLY BENEFIT (20, 21) or substantially hinder (7, 10, 30) glycemic control, depending on the quantity consumed, and these contrasting effects are reflected by alterations in postprandial hepatic glycogen synthesis. Low levels of dietary fructose activate glucokinase, thereby promoting direct pathway conversion of glucose into glycogen and enhancing net hepatic glucose uptake (19). In contrast, high fructose intake is characterized by its unregulated conversion into triose phosphates (triose-P) that in turn promote excessive gluconeogenic and lipogenic fluxes (5, 30). In the postprandial state, triose-P fluxes can also support high indirect pathway fluxes of glycogen synthesis competing with glycogenesis from glucose, thereby reducing net hepatic glucose uptake. Therefore, the contributions of dietary fructose and glucose to hepatic glycogen synthesis fluxes inform the distinction between catalytic levels of dietary fructose that are benefic...

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“…40 Reduced hepatic parasympathetic activity has already been suggested as one of the mechanisms underlying insulin resistance in sucrose-fed rats. 41 A limitation of the present study was that we were not able to evaluate autonomic balance to other targets, such as the liver and skeletal muscle. Future studies will be necessary to address the mechanisms underlying Ang-(1-7) effects on glucose metabolism.…”

mentioning

confidence: 94%

Increasing Angiotensin-(1–7) Levels in the Brain Attenuates Metabolic Syndrome–Related Risks in Fructose-Fed Rats

et al. 2014

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Metabolic syndrome (MetS) is currently recognized as a worldwide health problem, 1,2 and the substantial increase in fructose intake in human diet, especially as high-fructose corn syrup, has been considered a potential factor predisposing humans to MetS. 3,4 MetS is a cluster of different risk factors, such as increase in visceral fat deposition, glucose intolerance, dyslipidemia, and hypertension, which increases the risk of development of cardiovascular and renal diseases and type II diabetes mellitus. 2,5 Recent studies in rodents have shown that the renin-angiotensin system, through the inappropriate overactivity of angiotensin (Ang) II on Ang II type 1 (AT 1 ) receptor especially in the circulation and in the white adipose tissue, plays a pivotal role on the pathogenesis of MetS. [6][7][8] Peripheral blockade of Ang II synthesis or its action on AT 1 receptor attenuates metabolic disorders in obese rodents. [6][7][8] In contrast, the other functional arm of renin-angiotensin system, represented by the actions of Ang-(1-7) on Mas receptor, has been recognized widely as a counter-regulatory axis of Ang II/AT 1 receptor actions.Recent studies have shown that chronic increases in peripheral Ang-(1-7)/Mas receptor activity play a protective role in the regulation of cardiovascular and energy metabolism. Transgenic rats with increased Ang-(1-7) levels in the circulation [TGR(A1-7)3292] are protected against cardiac dysfunction, fibrosis, and hypertension when subjected to deoxycorticosterone (DOCA) acetate-salt model 9 and have enhanced resting glucose and lipid metabolism. 10 Accordingly, Giani et al 11,12 showed that chronic subcutaneous infusion of Ang-(1-7) improved insulin resistance, hypertension, and cardiac remodeling in fructose-fed rats. However, genetic deletion of Mas receptor alters glucose and lipid metabolism and the neural control of blood pressure, inducing a state of MetS. [13][14][15] Taken together, these data provide a clear evidence of a protective role of peripheral Ang-(1-7)/Mas receptor axis in the regulation of cardiovascular system and energy metabolism.Our group showed recently that chronic increase in Ang-(1-7) levels in the brain attenuates DOCA-salt hypertension, and that this effect is related to a dramatic beneficial role Abstract-We evaluated effects of chronic intracerebroventricular infusion of angiotensin (Ang)-(1-7) on cardiovascular and metabolic parameters in fructose-fed (FF) rats. After 6 weeks of fructose intake (10% in drinking water), SpragueDawley rats were subjected to intracerebroventricular infusion of Ang-(1-7) (200 ng/h; FF+A7 group) or 0.9% sterile saline (FF group) for 4 weeks with continued access to fructose. Compared with control rats, FF rats had increased mean arterial pressure and cardiac sympathetic tone with impaired baroreflex sensitivity. FF rats also presented increased circulating triglycerides, leptin, insulin, and glucose with impaired glucose tolerance. Furthermore, relative weights of liver and retroperitoneal adipose tissue were increased...

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Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves

Cited by 59 publications

References 33 publications

Heart Rate Variability, Insulin Resistance and Insulin Sensitivity in Japanese Adults: The Toon Health Study.

Heart Rate Variability, Insulin Resistance and Insulin Sensitivity in Japanese Adults: The Toon Health Study.

²H enrichment distribution of hepatic glycogen from²H₂O reveals the contribution of dietary fructose to glycogen synthesis

Increasing Angiotensin-(1–7) Levels in the Brain Attenuates Metabolic Syndrome–Related Risks in Fructose-Fed Rats

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Insulin resistance induced by sucrose feeding in rats is due to an impairment of the hepatic parasympathetic nerves

Cited by 59 publications

References 33 publications

Heart Rate Variability, Insulin Resistance and Insulin Sensitivity in Japanese Adults: The Toon Health Study.

Heart Rate Variability, Insulin Resistance and Insulin Sensitivity in Japanese Adults: The Toon Health Study.

2H enrichment distribution of hepatic glycogen from2H2O reveals the contribution of dietary fructose to glycogen synthesis

Increasing Angiotensin-(1–7) Levels in the Brain Attenuates Metabolic Syndrome–Related Risks in Fructose-Fed Rats

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²H enrichment distribution of hepatic glycogen from²H₂O reveals the contribution of dietary fructose to glycogen synthesis