Electrical stimulation of the ventromedial hypothalamus enhances both fat utilization and metabolic rate that precede and parallel the inhibition of feeding behavior

Ruffin, Marie-Pierre; Nicolaı̈dis, Stylianos

doi:10.1016/s0006-8993(99)01922-8

Cited by 91 publications

(72 citation statements)

References 29 publications

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“…The neurochemical phenotype of glucosensory neurons is uncertain; however, noradrenergic activity in the VMH was increased during an episode of induced hypoglycemia (3) and noradrenergic circuits in the VMH affect circulating concentrations of glucose and glucose-mobilizing hormones (46). Stimulation of VMH increased sympathetic efferent activity in the liver, hepatic glucose output (47,48), metabolic rate (49), and adrenal nerve activity (50). It is unclear from the present results whether activation of compensatory responses occurs in response to a relative change in interstitial glucose or an absolute change, such as reaching a threshold level.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Glucose in Rat Ventromedial Hypothalamus During Acute and Recurrent Hypoglycemia

et al. 2003

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The activity of neurons in the ventromedial hypothalamus (VMH) important for initiating compensatory responses to hypoglycemia is influenced by ambient glucose concentration. In the present study, we used in vivo microdialysis to evaluate interstitial glucose concentrations in rat VMH under various glycemic conditions. Using the zero-net-flux method, steady-state glucose concentration in the VMH was ϳ20% of blood glucose (ϳ1.4 mmol/l) in fed rats but ϳ14% of blood glucose (ϳ0.7 mmol/l) in overnight-fasted rats. During moderate hypoglycemia VMH glucose declined in parallel with blood glucose; however, VMH glucose decreased to a greater degree than blood glucose during a more severe hypoglycemic episode, falling to 10 ؎ 1.2% of blood levels (P < 0.01). To determine whether VMH glucose concentrations were influenced by recurrent episodes of hypoglycemia a second zero-net-flux study was conducted. Steady-state glucose concentrations in the VMH were ϳ20% lower after three episodes of recurrent hypoglycemia, a value 17.8 ؎ 0.8% of blood glucose, although the relative change in VMH glucose levels during the first and fourth hypoglycemic episodes were similar. From these results, we conclude that interstitial glucose concentrations in the VMH are not maintained at a constant level and are more dynamic than previously proposed.

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Section: Discussionmentioning

confidence: 99%

Extracellular Glucose in Rat Ventromedial Hypothalamus During Acute and Recurrent Hypoglycemia

et al. 2003

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“…A variety of studies have demonstrated that activation of the sympathetic nervous system can increase metabolic rate and fat consumption, leading to a reduction in body weight (30,32). The NGF/NGF receptor system could participate in this response to EV injection.…”

Section: Discussionmentioning

confidence: 99%

Effect of anti-NGF on ovarian expression of α₁- and β₂-adrenoceptors, TrkA, p75^NTR, and tyrosine hydroxylase in rats with steroid-induced polycystic ovaries

Manni¹,

Holmäng²,

Cajander³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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(PCO) in rats are associated with higher ovarian release and content of norepinephrine, decreased ␤2-adrenoceptors (ARs), and dysregulated expression of ␣1-AR subtypes, all preceded by an increase in the production of ovarian NGF. The aim of this study was to further elucidate the role of NGF in the ovaries by blocking the action of NGF during development of EV-induced PCO in rats. Control and EV-injected rats were treated with intraperitoneal injections of IgG (control and PCO groups) or with anti-NGF antibodies (anti-NGF and PCO anti-NGF groups) every third day for 5 wk starting from the day of PCO induction. Rat weight, estrous cyclicity, ovarian morphology, ovarian mRNA, and protein expression of ␣1-AR subtypes, ␤2-AR, the NGF receptor tyrosine kinase A (TrkA), p75 neurotrophin receptor (p75 NTR ), and tyrosine hydroxylase (TH) were analyzed. Ovaries in both PCO and PCO anti-NGF groups decreased in size as well as in number and size of corpora lutea. mRNA expression of ␣ 1a-AR and TrkA in the ovaries was lower, whereas expression of ␣ 1b-and ␣1d-AR and TH was higher, in the PCO group than in controls. Protein quantities of ␣ 1-ARs, TrkA, p75 NTR , and TH were higher in the PCO group compared with controls, whereas the protein content of ␤ 2-AR was lower. Anti-NGF treatment in the PCO group restored all changes in mRNA and protein content, except that of ␣ 1b-AR and TrkA mRNAs, to control levels. The results indicate that the NGF/NGF receptor system plays a role in the pathogenesis of EV-induced PCO in rats.nerve growth factors; sympathetic nervous system; ovarian innervation; tyrosine kinase A; p75 neutrophin receptor POLYCYSTIC OVARY SYNDROME (PCOS) is a heterogeneous condition of uncertain etiology that affects between 5% and 10% of women of reproductive age (41). PCOS is characterized by a myriad of symptoms and signs, which include ovulatory dysfunction, the presence of polycystic ovaries (PCO), abdominal obesity, hyperandrogenism, and in many cases hypertension and insulin resistance (41). Several theories have been proposed to explain the pathogenesis of PCOS, such as an enhanced production of ovarian androgens, an alteration in the metabolism of cortisol resulting in enhanced production of adrenal androgens, a defect in the action and secretion of insulin, and a neuroendocrine defect that causes an exaggeration in the pulse and frequency amplitude of LH (41).The involvement of the sympathetic nervous system in the etiology and maintenance of PCOS is suggested by both clinical and experimental findings (5,20,22,24,25). Ovarian function is known to be regulated by both hormonal and intraovarian signaling. It is also known that the sympathetic innervation of the ovary is involved in follicular development (23) and in ovarian steroidogenesis (1). That the sympathetic nervous system is involved in the pathophysiology of human PCOS is supported by the fact that the innervation of the catecholaminergic nerve fibers in the PCO of women with PCOS is more dense than in normal ovaries (18,35).Chronic anovulati...

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“…46,57 These effects may be related to autonomic changes due to VMH stimulation, which has been shown to increase metabolic rate. 94 This increase in energy expenditure was associated with increased fat oxidation given a concomitant drop in the respiratory quotient. Thus, heightened metabolism induced by VMH stimulation was sustained by utilization of fat stores, most likely due to noradrenergic turnover.…”

Section: Stereotaxy and Stimulation Of The Vmhmentioning

confidence: 99%

Deep brain stimulation in the treatment of obesity

Halpern¹,

Wolf²,

Bale

et al. 2008

JNS

140

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Obesity is a growing global health problem frequently intractable to current treatment options. Recent evidence suggests that deep brain stimulation (DBS) may be effective and safe in the management of various, refractory neuropsychiatric disorders, including obesity. The authors review the literature implicating various neural regions in the pathophysiology of obesity, as well as the evidence supporting these regions as targets for DBS, in order to explore the therapeutic promise of DBS in obesity.The lateral hypothalamus and ventromedial hypothalamus are the appetite and satiety centers in the brain, respectively. Substantial data support targeting these regions with DBS for the purpose of appetite suppression and weight loss. However, reward sensation associated with highly caloric food has been implicated in overconsumption as well as obesity, and may in part explain the failure rates of conservative management and bariatric surgery. Thus, regions of the brain's reward circuitry, such as the nucleus accumbens, are promising alternatives for DBS in obesity control.The authors conclude that deep brain stimulation should be strongly considered as a promising therapeutic option for patients suffering from refractory obesity. 625Abbreviations used in this paper: BMI = body mass index; DBS = deep brain stimulation; GABA = γ-aminobutyric acid; LH = lateral hypothalamus; MCH = melanin-concentrating hormone; NAc = nucleus accumbens; OCD = obsessive-compulsive disorder; PD = Parkinson disease; 6-OHDA = 6-hydroxydopamine; STN = subthalamic nucleus; VMH = ventromedial hypothalamus; VP = ventral pallidum.

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Electrical stimulation of the ventromedial hypothalamus enhances both fat utilization and metabolic rate that precede and parallel the inhibition of feeding behavior

Cited by 91 publications

References 29 publications

Extracellular Glucose in Rat Ventromedial Hypothalamus During Acute and Recurrent Hypoglycemia

Extracellular Glucose in Rat Ventromedial Hypothalamus During Acute and Recurrent Hypoglycemia

Effect of anti-NGF on ovarian expression of α₁- and β₂-adrenoceptors, TrkA, p75^NTR, and tyrosine hydroxylase in rats with steroid-induced polycystic ovaries

Deep brain stimulation in the treatment of obesity

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Electrical stimulation of the ventromedial hypothalamus enhances both fat utilization and metabolic rate that precede and parallel the inhibition of feeding behavior

Cited by 91 publications

References 29 publications

Extracellular Glucose in Rat Ventromedial Hypothalamus During Acute and Recurrent Hypoglycemia

Extracellular Glucose in Rat Ventromedial Hypothalamus During Acute and Recurrent Hypoglycemia

Effect of anti-NGF on ovarian expression of α1- and β2-adrenoceptors, TrkA, p75NTR, and tyrosine hydroxylase in rats with steroid-induced polycystic ovaries

Deep brain stimulation in the treatment of obesity

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Effect of anti-NGF on ovarian expression of α₁- and β₂-adrenoceptors, TrkA, p75^NTR, and tyrosine hydroxylase in rats with steroid-induced polycystic ovaries