The effects of stimulation and lesioning of afferent nerves on blood glucose and free fatty acid contents in rats in conditions of changing glycemia

Spiridonov, V. K.; Vorob'eva, N. F.

doi:10.1007/bf02463160

Cited by 4 publications

(3 citation statements)

References 15 publications

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“…A link between circulating FFAs and resistin is less clear, but correlation analysis in mice suggests an interaction between high circulating resistin levels with hyperlipidemia, as well as with obesity and insulin resistance [29]. Our results are in agreement with Spiridonov and Vorobeva [30], who also reports decreased FFA levels after neonatal treatment. Typically, higher levels of FFA are associated with disturbances in glucose homeostatic mechanisms [31] and this could mean that decreased levels of FFA contribute to the enhanced glucose disposal in CAP rats in following fuel excursions.…”

Section: Discussionsupporting

confidence: 90%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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Several mechanisms involved in ingestive behavior and neuroendocrine activity rely on vagal afferent neuronal signaling. Seemingly contradictory to this idea are observations that vagal afferent neuronal ablation by neonatal capsaicin (CAP) treatment has relatively small effects on glucose homeostasis and long-term regulation of energy balance. It may be proposed that humoral endocrine factors and/or their sensitivities compensate for the loss of vagal afferent information, particularly when subjects face disturbances in ambient fuel levels. Therefore, male adult rats neonatally treated with CAP or with the vehicle (VEH) underwent intravenous glucose tolerance tests (IVGTTs) during which blood fuel levels, and circulating adipose, pancreatic, and adrenal hormones were assessed. CAP rats displayed similar hyperglycemia as VEH rats, but with markedly reduced plasma insulin and corticosterone responses. These results indicate that CAP rats have increased insulin sensitivity during hyperglycemic episodes, and lower plasma levels of corticosterone in CAP rats relative to VEH rats could underlie this effect. After the IVGTT, CAP rats had increased plasma adiponectin and reduced plasma resistin levels, and these alterations in adipose hormones might be relevant for post-ingestive metabolic processes. In a second experiment, anorexigenic efficacies of cholecystokinin and leptin were assessed. While VEH rats, but not CAP rats, responded with reduced food intake to i.p. injected cholecystokinin, only CAP rats responded to i.v. infused leptin with a reduction in food intake. It is concluded that reduced HPA axis activity and/or increased leptin signaling could underlie compensations in fuel handling and energy balance following CAP treatment.

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Section: Discussionsupporting

confidence: 90%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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“…The HVAN also regulates insulin sensitivity ( Spiridonov and Vorob’eva, 2000 ). Hepatic vagotomy acutely reduces insulin sensitivity in lean rats, decreasing skeletal muscle glucose clearance by 45% ( Fernandes et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte membrane potential regulates serum insulin and insulin sensitivity by altering hepatic GABA release

et al. 2021

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SUMMARY Hepatic lipid accumulation in obesity correlates with the severity of hyperinsulinemia and systemic insulin resistance. Obesity-induced hepatocellular lipid accumulation results in hepatocyte depolarization. We have established that hepatocyte depolarization depresses hepatic afferent vagal nerve firing, increases GABA release from liver slices, and causes hyperinsulinemia. Preventing hepatic GABA release or eliminating the ability of the liver to communicate to the hepatic vagal nerve ameliorates the hyperinsulinemia and insulin resistance associated with diet-induced obesity. In people with obesity, hepatic expression of GABA transporters is associated with glucose infusion and disposal rates during a hyperinsulinemic euglycemic clamp. Single-nucleotide polymorphisms in hepatic GABA re-uptake transporters are associated with an increased incidence of type 2 diabetes mellitus. Herein, we identify GABA as a neuro-hepatokine that is dysregulated in obesity and whose release can be manipulated to mute or exacerbate the glucoregulatory dysfunction common to obesity.

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“…FFA levels were not measured in the present study, although they may provide an index of adipose insulin sensitivity that may help explain the improvement of insulin sensitivity seen after RTX desensitization. Capsaicin-treated normal rats with increased insulin sensitivity have been shown to have reduced levels of nonesterified FFAs as well as an enhanced whole body lipogenesis (26,38). This might be connected to reduced levels of epinephrine, norepinephrine, glucagon, and corticosterone, which are all lipolytic (23,26) and should be further studied.…”

mentioning

confidence: 99%

Sensory nerve inactivation by resiniferatoxin improves insulin sensitivity in male obese Zucker rats

Moesgaard

Brand²,

Sturis³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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Recent studies have suggested that sensory nerves may influence insulin secretion and action. The present study investigated the effects of resiniferatoxin (RTX) inactivation of sensory nerves (desensitization) on oral glucose tolerance, insulin secretion and whole body insulin sensitivity in the glucose intolerant, hyperinsulinemic, and insulin-resistant obese Zucker rat. After RTX treatment (0.05 mg/kg RTX sc given at ages 8, 10, and 12 wk), fasting plasma insulin was reduced ( P < 0.0005), and oral glucose tolerance was improved ( P < 0.005). Pancreas perfusion showed that baseline insulin secretion (7 mM glucose) was lower in RTX-treated rats ( P = 0.01). Insulin secretory responsiveness to 20 mM glucose was enhanced in the perfused pancreas of RTX-treated rats ( P < 0.005) but unaffected in stimulated, isolated pancreatic islets. At the peak of spontaneous insulin resistance in the obese Zucker rat, insulin sensitivity was substantially improved after RTX treatment, as evidenced by higher glucose infusion rates (GIR) required to maintain euglycemia during a hyperinsulinemic euglycemic (5 mU·kg−1·min−1) clamp (GIR60–120min: 5.97 ± 0.62 vs. 11.65 ± 0.83 mg·kg−1·min−1 in RTX-treated rats, P = 0.003). In conclusion, RTX treatment and, hence, sensory nerve desensitization of adult male obese Zucker rats improved oral glucose tolerance by enhancing insulin secretion, and, in particular, by improving insulin sensitivity.

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The effects of stimulation and lesioning of afferent nerves on blood glucose and free fatty acid contents in rats in conditions of changing glycemia

Cited by 4 publications

References 15 publications

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Hepatocyte membrane potential regulates serum insulin and insulin sensitivity by altering hepatic GABA release

Sensory nerve inactivation by resiniferatoxin improves insulin sensitivity in male obese Zucker rats

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