A direct action of insulin on the hypothalamic satiety center

Debons, Albert F.; Krimsky, I.; From, Anat

doi:10.1152/ajplegacy.1970.219.4.938

Cited by 146 publications

(30 citation statements)

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“…Another line of evidence is based on the hyperphagia seen after injury to the VMH caused by administration of goldthioglucose (GTG) [2,6,7,8,9,10,15,20,25,27]. It has been suggested that VMH glucoreceptors are unable to distinguish between GTG and glucose, take up GTG and then pay the penalty for their mistake [19].…”

Section: Discussionmentioning

confidence: 99%

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Increased feeding in response to bilateral injection of insulin antibodies in the VMH

Strubbe¹,

Mein²

1977

Physiology & Behavior

153

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Section: Discussionmentioning

confidence: 99%

“…It has been suggested that VMH glucoreceptors are unable to distinguish between GTG and glucose, take up GTG and then pay the penalty for their mistake [19]. This view is strengthened by the fact that a normal plasma insulin level is needed for the entrance of GTG into the VMH neurons as appears from the work of Debons [7,8,10].…”

Section: Discussionmentioning

confidence: 99%

Increased feeding in response to bilateral injection of insulin antibodies in the VMH

Strubbe¹,

Mein²

1977

Physiology & Behavior

153

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“…The effect of insulin on the brain is less well defined. Elevations of circulating insulin can alter brain function, augmenting the counterregulatory response to hypoglycemia (Davis et al, 1993;FruewaldSchultes et al, 1999), altering feeding behaviour (Debons et al, 1970;Rodin et al, 1985), and modulating auditory evoked potentials (Kern et al, 1994). How insulin abnormalities may contribute to the symptoms and pathogenesis have been examined in various experimental model systems and role for insulin has been established in molecular and neurophysiological features of memory processing (Zhao and Alkon, 2001).…”

Section: Introductionmentioning

confidence: 99%

The Protective Effects of Insulin on Hydrogen Peroxide-Induced Oxidative Stress in C6 Glial Cells

Mahesh¹,

Kim²

2009

Biomolecules and Therapeutics

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-Insulin appears to play a role in brain physiology, and disturbances of cerebral insulin signalling and glucose homeostasis are implicated in brain pathology. The objective of the present study was to investigate the protective effects of insulin under conditions of oxidative stress induced by hydrogen peroxide (H2O2) in C6 glial cells. Insulin at concentration of 10 −7 M could prevent 12 h H2O2-induced cell death. The formation of reactive oxygen species (ROS), nitric oxide (NO) and 2-thiobarbituric acid-reactive substances (TBARS) were significantly scavenged by insulin pre-treatment in C6 glial cells after H 2 O 2 -induced oxidative stress. Insulin significantly stimulated the phosphorylation of Akt in the cells and the activation of Akt was maintained in response to insulin under H2O2 incubation for 12 h. In conclusion, these results provide evidence that insulin acts as a free radical scavenger and stimulating Akt activity. These data suggest that insulin may be effective in degenerative diseases with oxidative stress.

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“…Infusions ofinsulin into the cerebral ventricle have been reported to decrease food intake in baboons (2) and in rats (3). Injection of insulin into the cerebral vesicles (4,5), into the hypothalamus itself (6)(7)(8), or into the carotid artery (9) can decrease blood sugar. More directly, Oomura and Kita (10) have shown that iontophoretic application ofinsulin into the ventromedial hypothalamus (VMH) reduced the discharge rate of glucoreceptor neurons.…”

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confidence: 99%

Intrahypothalamic injection of insulin decreases firing rate of sympathetic nerves.

Takeo¹,

Bray²

1987

Proc. Natl. Acad. Sci. U.S.A.

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Injection of picomolar quantities of insulin into the ventromedial hypothalamus of rats sgicandy reduced the firing rate of sympathetic nerves that supply interscapular brown adipose tissue. The minimal ring rate was reached in 2 min, and the effect was gone within 4 min. The effect of insulin was dose-related and did not occur when comparable volumes of physiological saline were injected into the ventromedial hypothalamus. Destruction of neurons in the ventromedial hypothalamus by ijection of kainic acid abolished the inhibitory effects of insulin. These data suggest that insulin may play a role in modulating the sympathetic firing rate to thermogenically important tissues.Since the demonstration by Bernard (1) more than 100 years ago that piqlre of the midbrain could produce diabetes in experimental animals, the hypothalamus has been a site of interest for diabetologists. The hypothesis that the hypothalamus might respond directly to insulin is supported by several studies. Infusions ofinsulin into the cerebral ventricle have been reported to decrease food intake in baboons (2) and in rats (3). Injection of insulin into the cerebral vesicles (4, 5), into the hypothalamus itself (6-8), or into the carotid artery (9) can decrease blood sugar. More directly, Oomura and Kita (10) have shown that iontophoretic application ofinsulin into the ventromedial hypothalamus (VMH) reduced the discharge rate of glucoreceptor neurons. When glucose or glucose plus insulin were added to the same neurons, the electrical discharge rate increased (10, 11).The VMH can modulate both the parasympathetic and sympathetic nervous systems (12). Electrical stimulation of the VMH increases the activity of the sympathetic nerves to brown adipose tissue (13,14 MATERIALS AND METHODS Animals. Twenty-two male Wistar rats (250-300 g) were used in these studies. They were fed a standard diet (Oriental Yeast M10, Osaka, Japan) with free access to tap water and were housed individually in a room maintained at 19 ± 30C.Hypothalamic Lesions. After anesthesia with pentobarbital (45 mg/kg), animals were mounted in a stereotaxic apparatus.Twenty-two-gauge guide cannulas were aimed at +6.0 mm anteriorly, ±1.0 mm laterally, and -3.5 to 4.0 mm below the zero plane in the VMH, using the coordinates ofPellegrino et al. (16). These cannulas were inserted through burr holes and anchored to the skull with dental cement and stainless steel screws. Twelve of the 22 rats received injections of kainic acid through a 28-gauge needle inserted through the 22-gauge guide cannulas. The kainic acid (Sigma) was dissolved in physiological saline (0.15 M NaCl), and 0.8 ,ul of a 1.0 ,AM solution of kainic acid was infused into the VMH over 2 1/2 min. The 28-gauge cannula was left in place for an additional 2 min. The remaining 10 animals received saline and served as sham-lesioned controls.Nerve Recording. Sympathetic nerve recordings were performed 6-9 days after the implantation of the guide cannula and injection of kainic acid or saline. Anesthesia was induced by ...

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A direct action of insulin on the hypothalamic satiety center

Cited by 146 publications

References 0 publications

Increased feeding in response to bilateral injection of insulin antibodies in the VMH

Increased feeding in response to bilateral injection of insulin antibodies in the VMH

The Protective Effects of Insulin on Hydrogen Peroxide-Induced Oxidative Stress in C6 Glial Cells

Intrahypothalamic injection of insulin decreases firing rate of sympathetic nerves.

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