Neuroendocrine and amine studies in affective illness

Casper, Regina C.; Davis, John M.; Pandey, Ghanshyam N.; Garver, David L.; Dekirmenjian, H.

doi:10.1016/0306-4530(77)90016-6

Cited by 82 publications

(24 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An association between insulin resistance (IR) and affective disorders has been postulated in a number of cross-sectional studies [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17]. Limited data exist on potential changes in IR associated with improvement in depressive symptoms and/or depression remission resolutiontwo studies reported decreased IR after successful antidepressant treatment [1,18], while another study reported persisting IR even after successful treatment [15].…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone Add-On in Treatment of Depressed Patients with Insulin Resistance: a Pilot Study

Rasgon

Kenna

Williams

et al. 2010

The Scientific World JOURNAL

View full text Add to dashboard Cite

A number of cross-sectional studies have suggested an association between insulin resistance (IR) and affective disorders. However, limited data exist on potential changes in IR in a prospective treatment of depression. The present pilot study tested the hypothesis that improvement of IR with the addition of an insulin-sensitizing agent would improve mood in nondiabetic patients with unipolar or bipolar depression, who had surrogate blood markers suggestive of IR. Surrogate IR-criteria blood markers were fasting plasma glucose >100 mg/dl or triglyceride (TG) to high density lipoprotein (HDL) ratio >3.0. Open-label rosiglitazone, titrated to a dose of 8 mg/day, was administered for 12 weeks to 12 patients with depressive disorder receiving treatment as usual (TAU). Eight patients who completed the 12-week study exhibited significant declines in both depression severity by the Hamilton Depression Rating Scale and the Clinical Global Impression scale, with moderate effect sizes noted. Modest improvement in Matsuda Index scores was also noted at 12 weeks, yet declines in depression severity scores were not associated with improvements in the endocrine markers (Matsuda Index, TG/HDL ratio, and body mass index). These results suggest the potential novel use for an insulin-sensitizing agent in the treatment of depressive disorders. Larger placebo-controlled studies are warranted.

show abstract

Section: Introductionmentioning

confidence: 99%

Rosiglitazone Add-On in Treatment of Depressed Patients with Insulin Resistance: a Pilot Study

Rasgon

Kenna

Williams

et al. 2010

The Scientific World JOURNAL

View full text Add to dashboard Cite

show abstract

“…Various reports in the literature show reduced re sponses to GHRH [Lesch et al, 1987[Lesch et al, , 1988, clonidine [Ansseau et al, 1988;Lesch et al, 1988] and ITT [Mueller et al, 1969;Casper et al, 1977] in depressed patients; on the other hand, increased responsiveness to GHRH [Baranowska et al, 1986;Masuda et al, 1988], normal or increased effects of clonidine [Brambilla et al, 1987[Brambilla et al, , 1989 and reduced GH responses to ITT [Nakagawa et al, 1985;Baranowska et al, 1986] have been shown in anorexic women. These findings suggested the presence of a hypothalamic-pituitary disorder in the reg ulation of GH secretion in these illnesses.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, patients affected by these psychiatric disorders show elevated 24-hour circulating levels of adrenocorticotropin (ACTH) and cortisol [Linkowski et al, 1985;Mortola et al, 1987Mortola et al, , 1989], a blunted ACTH-cortisol response to the administration of exoge nous corticotropin-releasing hormone (CRH) [Gold et al, 1986a, b;Mortola et al, 1989] and nonsuppressed cortisol responses to dexamethasone suppression test [Danowski et al, 1972;Carroll et al, 1976;Gwirstman et al, 1983;Kiriike et al, 1986]. Furthermore, blunted or delayed thyroid-stimulating hormone (TSH) re sponses to thyrotropin-releasing hormone (TRH) have been reported in bulimia [Gwirstman et al, 1983;Norris et al, 1985;Kiriike et al, 1987;, anorexia nervosa [Norris et al, 1985;Kiriike et al, 1987;Kiyohara et al, 1987] and depression [Loosen and Prange, 1982], Concerning growth hormone (GH) secre tion, an anomalous GH responsiveness to TRH has been found in all of these psychiatric disorders [Maeda et al, 1976;Gold et al, 1981;Gwirstman et al, 1983;Kiriike et al, 1987;, In addition, studies of GH release induced by normally acting stimuli such as GHreleasing hormone (GHRH), clonidine or hypoglycemia have shown a disturbed hypothalamic pituitary regula tion of GH secretion in anorexic [Landon et al, 1966;Nakagawa et al, 1985;Baranowska et al, 1986;Masuda et al, 1988;Brambilla et al, 1989] and depressed [Mueller et al, 1969;Casper et al, 1977;Lesch et al. 1987;Ansseau et al, 1988;Lesch et al, 1988] patients.…”

Section: Introductionmentioning

confidence: 99%

Growth Hormone Responses to Growth Hormone-Releasing Hormone, Clonidine and Insulin-Induced Hypoglycemia in Normal Weight Bulimic Women

Coiro

Capretti²,

Volpi³

et al. 1990

Neuropsychobiology

View full text Add to dashboard Cite

The growth hormone (GH) responses to GH-releasing hormone (GHRH; 1 μg/kg BW in an i.v. bolus), clonidine (150 μg in a single oral dose) and insulin (0.15 IU/kg BW in an i.v. bolus) induced hypoglycemia were evaluated in 7 normal weight bulimic women with regular menstrual cycles and in 7 age- and weight-matched normal women. In addition, the effect of thyrotropin-releasing hormone (TRH; 200 μg in an i.v. bolus) on serum thyroid-stimulating hormone (TSH) and GH levels was measured in the same subjects. Tests were carried out in random order on the 22nd days of the following menstrual cycles. A control test with the i.v. administration of normal saline instead of drugs was carried out 2 days after the TRH test. Basal GH levels were significantly higher in bulimic women than in normal controls; despite higher GH levels, bulimic women showed normal circulating concentrations of somatomedin-C (Sm-C). Serum GH levels remained unmodified during the control test. In contrast, the administration of GHRH, clonidine or insulin induced significant GH responses in all subjects. Bulimic and normal women showed comparable responses after GHRH, clonidine or hypoglycemia. The hypoglycemic response to insulin was similar in bulimic and control subjects. The administration of TRH was unable to increase the circulating levels of GH in the normal controls, whereas it significantly increased GH concentrations in 5 of 7 bulimic women. Delayed TSH responses to TRH were observed in the bulimic group. These data indicate that normal weight bulimia is not accompanied by abnormalities in the hypothalamic pituitary responsiveness to normally acting GH-releasing stimuli. Taken together with the finding of normal plasma Sm-C levels, these results suggest the integrity of the GHRH-GH-somatomedin axis in bulimia. On the other hand, the anomalous effects of TRH suggest an abnormal sensitivity of the GH and TSH secretory systems to TRH in bulimia.

show abstract

“…As for the urinary output of MHPG, the noradrenaline metabolite of the nervous system, Schildkraut (83,85), Maas and his colleagues (25,50,51), and Casper et al (13), claim that it is excreted in abnormally low amounts in depressed patients. This is all the more interesting because in some studies other catecholamine metabolites measured at the same time, such as metanephrine, normetanephrine and VMA, were present in the usual amounts.…”

Section: Noradrenalinementioning

confidence: 99%

“…There is an indirect piece of evidence from neuroendocrinology pointing to deficient dopaminergic mechanisms in the hypothalamus of depressed patients. Hypoglycemia calls these mechanisms into play with a resultant increase in secretion of growth hormone, but the response is subnormal in depression (13).…”

Section: Dopaminementioning

confidence: 99%

Biochemistry of Mental Depression

Sourkes

1977

Canadian Psychiatric Association Journal

View full text Add to dashboard Cite

Neuroendocrine and amine studies in affective illness

Cited by 82 publications

References 10 publications

Rosiglitazone Add-On in Treatment of Depressed Patients with Insulin Resistance: a Pilot Study

Rosiglitazone Add-On in Treatment of Depressed Patients with Insulin Resistance: a Pilot Study

Growth Hormone Responses to Growth Hormone-Releasing Hormone, Clonidine and Insulin-Induced Hypoglycemia in Normal Weight Bulimic Women

Biochemistry of Mental Depression

Contact Info

Product

Resources

About