The Effects of Improved Blood Glucose on Growth Hormone and Cortisol Secretion in Insulin‐dependent Diabetes Mellitus

Würzburger, M. I.; Prelević, Gordana M.; Ph, Sönksen; Perić, Leon; Till, Stephen J.; Morris, Richard W

doi:10.1111/j.1365-2265.1990.tb00926.x

Cited by 40 publications

(29 citation statements)

References 20 publications

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“…As discussed earlier, in vitro studies have implicated these hormones as requirements for optimal milk supply (6,(8)(9)(10)(11)(12)(13)(14)(15)17); however, information is lacking in regard to their corrective roles in vivo. In the present study, the levels of corticosterone, unlike previous works, were not altered by the degree of diabetes induced here nor by the insulin treatments used (39)(40)(41)(42)56). However, comparison is made difficult as male and female nonlactators were used in the aforementioned studies versus lactators in the present one.…”

Section: Discussioncontrasting

confidence: 71%

Effects of Diabetes Mellitus on Lactation in the Rat

Lau

Sullivan

Hazelwood

1993

Experimental Biology and Medicine

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Diabetes mellitus adversely affects the process of lactation. Although insulin administration restores lactation, the manner by which it does so is unknown. The goals of this study were to determine which phase of lactation, milk synthesis/supply (MS), and/or milk release (MR) was affected. Inasmuch as insulin, corticosterone, and prolactin, among other hormones, are involved in milk synthesis in vitro, this study investigated their probable roles in the suppression of lactation in diabetes in vivo. Diabetes was induced in rats on Day 3 postpartum with streptozotocin (50-60 mg/kg, ip). Milk synthesis/supply and milk release were indirectly monitored using body weight gain of pups during a timed-feeding period on postnatal Days 8/9 and 13/14. Plasma corticosterone, insulin, C-peptide, and prolactin were measured by radioimmunoassay in control, diabetic, and insulin-replaced diabetic animals. Insulin replacement was provided by means of an osmotic minipump implanted subcutaneously in the nape of the neck. In addition, several parameters of maternal behavior were monitored in order to determine whether diabetes affected maternal behavior and, therefore, whether such changes played a role in the alterations of lactation observed during diabetes. Diabetes significantly suppressed MS and MR. However, the decrease in MR, which was restored after partial insulin replacement, was a reflection of the reduced MS. There were no significant differences between the parameters of maternal behavior monitored in control and diabetic animals. Blood glucose in diabetic dams was significantly increased over that of controls. Although the levels of plasma glucose in the insulin-replaced groups were significantly lower than those of their uncontrolled diabetic counterparts, they also remained higher than that of controls. Corticosterone was not significantly altered after induction of diabetes. Insulin and C-peptide levels were significantly reduced in the uncontrolled diabetics; however, insulin levels were corrected in the insulin-replaced groups. Serum levels of prolactin decreased in all diabetic groups and insulin failed to restore these levels to those of control animals. In conclusion, it appears that diabetes decreases lactation through a suppressive effect on MS rather than on MR, with insulin replacement correcting for such deficiency. In addition, despite the lactogenic importance of glucocorticoids, prolactin and insulin demonstrated in vitro, lactation in vivo can be corrected without returning the levels of all three hormones to normal. The importance of another factor(s), such as normoglycemia, as essential to the observed defects, needs to be investigated.

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Section: Discussioncontrasting

confidence: 71%

Effects of Diabetes Mellitus on Lactation in the Rat

Lau

Sullivan

Hazelwood

1993

Experimental Biology and Medicine

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“…A link between metabolic disorders and increased susceptibility to stress has been described (20,46,47). In particular, insulin-dependent diabetic patients show disruptions in HPA axis responsiveness (32,48), and a strong correlation among perceived stress, immunological status, and glycemic control has been described (49). In addition, diabetic patients show a higher incidence of affective, depressive, and anxiety disorders (50, 51) Experimental Diabetes, Hippocampal Vulnerability, and Glucose Homeostasis.…”

Section: Stz-treated Rats As a Model Of Endogenous Allostatic Loadmentioning

confidence: 99%

Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress

Magariños

McEwen

2000

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

244

160

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We report that 9 d of uncontrolled experimental diabetes induced by streptozotocin (STZ) in rats is an endogenous chronic stressor that produces retraction and simplification of apical dendrites of hippocampal CA3 pyramidal neurons, an effect also observed in nondiabetic rats after 21 d of repeated restraint stress or chronic corticosterone (Cort) treatment. Diabetes also induces morphological changes in the presynaptic mossy fiber terminals (MFT) that form excitatory synaptic contacts with the proximal CA3 apical dendrites. One effect, synaptic vesicle depletion, occurs in diabetes as well as after repeated stress and Cort treatment. However, diabetes produced other MFT structural changes that differ qualitatively and quantitatively from other treatments. Furthermore, whereas 7 d of repeated stress was insufficient to produce dendritic or synaptic remodeling in nondiabetic rats, it potentiated both dendritic atrophy and MFT synaptic vesicle depletion in STZ rats. These changes occurred in concert with adrenal hypertrophy and elevated basal Cort release as well as hypersensitivity and defective shutoff of Cort secretion after stress. Thus, as an endogenous stressor, STZ diabetes not only accelerates the effects of exogenous stress to alter hippocampal morphology; it also produces structural changes that overlap only partially with those produced by stress and Cort in the nondiabetic state.A drenal glucocorticoids (GCs) are major mediators of the adaptive response to stress, and they also play a crucial role in feedback mechanisms that contain or protect against defense reactions that are activated by stress, such as inflammation (1, 2). The process of adaptation to environmental demands, also called ''allostasis'' (3, 4), functions best when stress mediators such as those associated with the activation of the hypothalamo-pituitaryadrenal (HPA) axis are turned on efficiently when needed and turned off again when not needed (5). When HPA activity is elevated chronically or managed inefficiently, various forms of pathophysiology are accelerated, such as bone mineral loss, loss of muscle protein mass, insulin resistance, and dysfunction of the hippocampal region of the brain (5, 6). This cost to the body has been termed ''allostatic load' ' (4, 5). MRI studies in stress-related disorders, such as posttraumatic stress disorder, recurrent depressive illness, Cushing's syndrome, and mild cognitive impairment in aging patients, have revealed atrophy of the human hippocampus accompanied by deficits in declarative and spatial memory (7-11), in line with the recognized role of the hippocampus in cognitive processes (12). However, the exact nature of the atrophy is unclear, whether it is caused by permanent damage or by a potentially reversible form of plasticity.In experimental animals, severe and prolonged stress or GC administration has been reported to cause brain damage associated with hippocampal neuronal loss (see ref. 6 for review). We have described previously that shorter periods of repeated stress alter hippocamp...

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“…As chil dren were fed immediately four safety reasons at the camp when BG was below 3.3 mmol/1, the expected GH increase may have been suppressed by increasing BG lev els [24], GH levels are typically elevated in cases of poorly con trolled IDDM and can be reduced by intensive insulin 207 treatment [1,25,26], We could not demonstrate a rela tionship between HbAjC and individual mean GH levels because the patients were in a narrow' range of moderate glycaemic control.…”

Section: Discussionmentioning

confidence: 77%

Urinary Growth Hormone Excretion in Diabetic Children: Relation to Nocturnal Course of Blood Glucose Levels

et al. 1993

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A potential relation was evaluated between nocturnal urinary growth hormone (GH) excretion as a parameter for integrated GH secretion and the course of blood glucose (BG) levels during night and morning hours. Twelve diabetic children aged 11.6 ± 2.0 years (mean ± SD), with diabetes duration 4.4 ± 1.6 years, took part in the study. Urine for GH estimation by a highly sensitive EIA was collected from 24.00 to 07.00 h during a diabetic summer camp. BG was monitored at 24.00, 04.00 and 07.00 h. Mean nocturnal GH excretion measured from 158 collections was 5.6 ± 5.1 ng/g creatinine, with a wide range of 0.36-36.6. Remarkable intra-individual variations were found between distinct nights. GH excretion correlated positively with BG levels at 07.00 h (p = 0.003) and with the increment of BG between 24.00 and 07.00 h (p = 0.002). Thus, endogenous variations in nocturnal GH levels may be involved in the day-to-day fluctuations in fasting BG in diabetic subjects.

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The Effects of Improved Blood Glucose on Growth Hormone and Cortisol Secretion in Insulin‐dependent Diabetes Mellitus

Cited by 40 publications

References 20 publications

Effects of Diabetes Mellitus on Lactation in the Rat

Effects of Diabetes Mellitus on Lactation in the Rat

Experimental diabetes in rats causes hippocampal dendritic and synaptic reorganization and increased glucocorticoid reactivity to stress

Urinary Growth Hormone Excretion in Diabetic Children: Relation to Nocturnal Course of Blood Glucose Levels

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