Divergent effect of dehydroepiandrosterone on energy intakes of Zucker rats

Wright, Bruce E.; Browne, Elizabeth; Švec, František; Porter, Johnny R.

doi:10.1016/0031-9384(93)90008-4

Cited by 23 publications

(20 citation statements)

References 13 publications

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“…This increment is blocked by the administration of DHEA. This site of action (LH) is consistent with some of our past results where we found that DHEA altered serotonin in the LH (26) and with the findings Fig. 2.…”

Section: Discussionsupporting

confidence: 94%

“…Second, more detailed analysis showed that serotonin was elevated specifically in the lateral hypothalamus (LH) of such animals and decreased within 24 h of discontinuing DHEA (13). Third, when DHEA was given as an intraperitoneal injection to animals consuming chow, serotonin levels increased in the LH of the obese animal but not in other hypothalamic regions (26). An acute intraperitoneal injection of DHEA to obese female Zucker rats that had been consuming a macronutrient selection diet caused an elevation of serotonin and 5-hydroxyindole-3-acetic acid (5-HIAA) in the paraventricular nuclear (PVN) region (20).…”

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confidence: 98%

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The influence of dehydroepiandrosterone and 8-OH-DPAT on the caloric intake and hypothalamic neurotransmitters of lean and obese Zucker rats

Porter

Vrancken

Corll

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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The 5 HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetraline (8-OH-DPAT) increases the food intake of satiated Zucker rats, both lean and obese. Associated with this increased intake are changes in the hypothalamic content of serotonin and its metabolite, 5-HIAA (5-hydroxyindole-3-acetic acid); serotonin is increased while the level of 5-HIAA is decreased. Analysis of individual 5-HIAA/5-hydroxytryptamine (5-HT) ratios, a measure of serotonin turnover indicate that 8-OH DPAT affected serotonin turnover equally and dramatically in both phenotypes. This would be an expected physiological action of an autofeedback mechanism by a 5-HT(1A) receptor agonist. Dehydroepiandrosterone (DHEA) at doses as low as 10 mg/kg blocks the 8-OH-DPAT-induced increase in food intake but does not alter food intake of control satiated Zucker rats. The mechanism of DHEA's action was investigated by monitoring the steroid's effect on hypothalamic neurotransmitters in this satiated model. DHEA by itself induced some change in 5-HIAA in the obese satiated model but not the lean. 8-OH-DPAT, by itself, dramatically decreased serotonin turnover in either lean or obese rats, and DHEA combined with 8-OH-DPAT did not further change serotonin turnover, suggesting DHEA may work through mechanisms other than monoamines to cause its inhibition of 8-OH-DPAT-induced behavioral effects at such low doses.

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Section: Discussionsupporting

confidence: 94%

mentioning

confidence: 98%

The influence of dehydroepiandrosterone and 8-OH-DPAT on the caloric intake and hypothalamic neurotransmitters of lean and obese Zucker rats

Porter

Vrancken

Corll

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Although several studies indicated that the anti-obesity effect of DHEA was associated with decreased food intake, no difference was observed in food consumption except for that in the first 2 weeks. It was suggested that DHEA-induced central neurotransmitter changes suppress the appetite; however, these changes may not persist longer than 3 weeks (45). Epidemiological studies suggest that high plasma DHEA-S level is associated with longevity (46,47), whereas, to our knowledge, our study is the first to provide evidence of the antiaging effect of DHEA.…”

Section: ) a L T H O U G H D O G U P T A K E B Y D H E A S T I M U mentioning

confidence: 50%

Effect of Dehydroepiandrosterone on Insulin Sensitivity and Adipocyte Growth in Otsuka Long-Evans Tokushima-Fatty Rats

Ishizuka¹,

Kajita²,

Fujioka³

et al. 2011

Topics in the Prevention, Treatment and Complications of Type 2 Diabetes

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“…The mechanism for this effect is unknown, as a specific DHEA-S receptor has not been identified. It is interesting that many studies have shown that DHEA and its sulfated ester can antagonize corticosteroid actions (22,24,25,36). The role of glucocorticoids in blunting physiological responses to stress are somewhat controversial, with a number of studies both supporting (11,17,19,37) and contradicting (14) this finding (10,13).…”

Section: Discussionmentioning

confidence: 79%

“…In Zucker rats, simultaneous infusion of DHEA and dexamethasone prevents the dexamethasone-induced increase in hepatic tyrosine aminotransferase activity (24). In addition, intracerebroventricular infusion of DHEA has been shown to increase norepinephrine and epinephrine levels in the paraventricular nucleus and ventromedial hypothalamus in obese Zucker rats (25). Although corticosteroids have been found to increase gluconeogenesis (26), proteolysis (27), and net fat deposition in humans (28), DHEA has been found to elicit the opposite effect on these metabolic processes (29 -32).…”

mentioning

confidence: 99%

The Effects of Dehydroepiandrosterone Sulfate on Counterregulatory Responses During Repeated Hypoglycemia in Conscious Normal Rats

et al. 2004

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We previously determined that both antecedent hypoglycemia and elevated cortisol levels blunt neuroendocrine and metabolic responses to subsequent hypoglycemia in conscious, unrestrained rats. The adrenal steroid dehydroepiandrosterone sulfate (DHEA-S) has been shown in several studies to oppose corticosteroid action. The purpose of this study was to determine if DHEA-S could preserve counterregulatory responses during repeated hypoglycemia. We studied 40 male Sprague-Dawley rats during a series of 2-day protocols. T he Diabetes Control and Complications Trial established that intensive glucose control in type 1 diabetic patients can slow the progression or significantly reduce the onset of diabetic microvascular complications (e.g., retinopathy, nephropathy, neuropathy) (1). Unfortunately, the study also established that intensive glucose treatment causes an approximate threefold increase in the frequency of severe hypoglycemia (2). This increased frequency of hypoglycemia is at least partially caused by deficient autonomic nervous system (ANS) counterregulatory responses to hypoglycemia (3-5). Repeated exposure to hypoglycemia reduces neuroendocrine, ANS, and metabolic (endogenous glucose production [EGP], lactate, and glycerol) counterregulatory responses to subsequent hypoglycemia by as much as 50% in nondiabetic and type 1 diabetic subjects (6 -9). These blunted counterregulatory responses are significant contributing factors to a vicious cycle of hypoglycemia for type 1 diabetic patients (9).The mechanisms responsible for the blunted counterregulatory responses seen after antecedent hypoglycemia are not fully understood. Controversy exists regarding the role played by corticosteroids in the pathophysiology of blunted ANS responses during hypoglycemia (10 -14). Reports in rodents (12) and humans (15) have demonstrated that, similar to antecedent hypoglycemia, antecedent increases of cortisol can blunt neuroendocrine and metabolic counterregulatory responses to next day hypoglycemia. In addition, patients with adrenocortical failure have preserved catecholamine, pancreatic polypeptide, glucagon, growth hormone, and muscle sympathetic nerve activity responses to hypoglycemia after antecedent hypoglycemia (16). Other animal studies have found that corticosteroids can blunt catecholamine responses to a variety of stressors, including insulin-induced hypoglycemia in sheep (17) and immobilization stress in rats (18,19). However, in contrast to the above studies, three other reports have indicated that prior corticosterone administration has little or no effect on ANS responses to subsequent hypoglycemia in the conscious rat (10,13,14).

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Divergent effect of dehydroepiandrosterone on energy intakes of Zucker rats

Cited by 23 publications

References 13 publications

The influence of dehydroepiandrosterone and 8-OH-DPAT on the caloric intake and hypothalamic neurotransmitters of lean and obese Zucker rats

The influence of dehydroepiandrosterone and 8-OH-DPAT on the caloric intake and hypothalamic neurotransmitters of lean and obese Zucker rats

Effect of Dehydroepiandrosterone on Insulin Sensitivity and Adipocyte Growth in Otsuka Long-Evans Tokushima-Fatty Rats

The Effects of Dehydroepiandrosterone Sulfate on Counterregulatory Responses During Repeated Hypoglycemia in Conscious Normal Rats

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