Increased Serum Growth Hormone and Somatic Growth in Adult Hamsters with Hippocampal Transections

Borer, Katarina T.; Kelch, Robert P.; Peugh, Janet; Huseman, Carol A.

doi:10.1159/000122901

Cited by 22 publications

(23 citation statements)

References 45 publications

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“…Completeness of pituitary removal was verified by examination of sella turcica under a dissecting microscope. Electro lytic lesions of rostromedial septum [6] and transections of hippo campus [7] were performed to induce rapid skeletal and somatic growth in adult hamsters as previously described.…”

Section: Methodsmentioning

confidence: 99%

Hamster Prolactin: Physiological Changes in Blood and Pituitary Concentrations as Measured by a Homologous Radioimmunoassay

Borer¹,

Kelch²,

Corley³

1982

Neuroendocrinology

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A specific and sensitive homologous radioimmunoassay (RIA) for determination of hamster prolactin is described and compared to heterologous hamster prolactin RIA and to the homologous and heterologous RIAs for rat prolactin. With this method, we have determined that, in the golden hamster, diurnal plasma prolactin fluctuations have a mean interpeak interval of 1.5 h, that serum prolactin concentrations are influenced by day length, by ether vapors, by animal’s gender, and by refeeding following a fast but not by neurosurgical procedures which increase somatic growth and serum GH concentration in adult hamsters. Variations in day length influenced pituitary prolactin content and concentration, and pituitary removal abolished prolactin secretory responses to ether stress. A heterologous RIA for hamster prolactin which utilizes radioiodinated rat prolactin and rabbit antihamster prolactin serum (RK1–15) represents the most advantageous method for the measurement of hamster prolactin because of its high sensitivity (0.14 ng/ml), high antiserum binding to iodinated rat prolactin, and the ability to measure both hamster and rat prolactin.

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Section: Methodsmentioning

confidence: 99%

Hamster Prolactin: Physiological Changes in Blood and Pituitary Concentrations as Measured by a Homologous Radioimmunoassay

Borer¹,

Kelch²,

Corley³

1982

Neuroendocrinology

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“…Several lines of experimental animal research confirm the inverse relationship between spontaneous physical activity and body fatness. Obesity induced by either VMH lesions in rats [23] , rostromedial septal lesions [290] and hippocampal [291] or septo-hypothalamic transections [292] in hamsters, or cafeteria and high-fat diets in neurologically intact animals [3,293,294] reduce spontaneous running activity. On the other hand, severe dietary restriction consisting of only 2-h access to food, leads to weight loss in rats and up to 300% to 500% increase in spontaneous running activity to the point of emaciation [295] .…”

Section: Body Mass Lossmentioning

confidence: 99%

“…[317] , and changes in body fat level are accompanied by changes in lean mass. In the hamster, rostral septal lesions [290] and hippocampal [291] and septo-hypothalamic [292] transections increase obesity but also elicit bone and lean body mass growth and an upward displacement of regulated body mass setpoint. Remarkably, increases in body mass setpoint without obesity also can be triggered by voluntary running in this species [318] proving Gordon Kennedy right about the interconnectedness of voluntary activity, weight regulation, and body growth [30,[319][320][321] .…”

mentioning

confidence: 99%

“…That this is a maturational event is seen by growth acceleration not being possible during animals' natural early rapid growth [323] . The requirement for growth cessation before the defenses of stable adult weight against downward deflections are initiated is shown by the necessity of pituitary gland presence for acceleration of growth by exercise [324] , increased pulsatile oversecretion of growth hormone during that growth [325,326] , and increased pulsatile growth hormone secretion after the disruption of the brain substrates involved in the maintenance of weight stability in nongrowing animals [290][291][292] . Finally, the permanence of neural changes involved in the defense of the growth-induced upward displacement of body mass setpoint is seen in the phenomenon of catch-up growth [325] .…”

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confidence: 99%

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Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Borer¹

2014

WJD

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A re-examination of the mechanism controlling eating, locomotion, and metabolism prompts formulation of a new explanatory model containing five features: a coordinating joint role of the (1) autonomic nervous system (ANS); (2) the suprachiasmatic (SCN) master clock in counterbalancing parasympathetic digestive and absorptive functions and feeding with sympathetic locomotor and thermogenic energy expenditure within a circadian framework; (3) interaction of the ANS/SCN command with brain substrates of reward encompassing dopaminergic projections to ventral striatum and limbic and cortical forebrain. These drive the nonhomeostatic feeding and locomotor motivated behaviors in interaction with circulating ghrelin and lateral hypothalamic neurons signaling through melanin concentrating hormone and orexin-hypocretin peptides; (4) counterregulation of insulin by leptin of both gastric and adipose tissue origin through: potentiation by leptin of cholecystokinin-mediated satiation, inhibition of insulin secretion, suppression of insulin lipogenesis by leptin lipolysis, and modulation of peripheral tissue and brain sensitivity to insulin action. Thus weight-loss induced hypoleptimia raises insulin sensitivity and promotes its parasympathetic anabolic actions while obesity-induced hyperleptinemia supresses insulin lipogenic action; and (5) inhibition by leptin of bone mineral accrual suggesting that leptin may contribute to the maintenance of stability of skeletal, lean-body, as well as adipose tissue masses.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Insulin; Leptin; Weight regulation; Autonomic; Circadian Core tip: The novel proposal for the mechanism of body weight regulation deals with all three components of body mass: bone, lean tissue, and fat depots. It attributes the central control of counterbalancing energy expenditure and intake to an autonomic nervous systemcircadian clock command center that encompases brain reward substrates, lateral hypothalamic peptidergic circuits and areas of the cortex. The nonhomeostatic character of feeding and locomotion is driven and controlled by the reward circuits and modulated by shifts in insulin sensitivity induced by counterregulation by leptin of insulin as weight deviates between underweight and overweight and alters basal leptin concentrations.Borer KT. Counterregulation of insulin by leptin as key component of autonomic regulation of body weight. World J Diabetes 2014; 5(5): 606-629 Available from:

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“…In the hamster, voluntary running levels are reduced by 80% following electrocoagulative lesions of rostromedial septum (10), horizontal transection of septo-hippocampal interconnections (9), or bilateral transections of dorsal hippocampus (11), while at the same time these neurosurgical procedures induce striking acceleration of somatic growth and some accumulation of body fat. These observations suggest that septo-hippocampal neural circuits participate in the bioenergetic modulation of spontaneous running in hamsters in that they suppress somatic growth and accumulation of fat at the same time that they stimulate spontaneous running activity.…”

Section: Fastingmentioning

confidence: 99%

Hippocampal serotonin mediates hypoactivity in dietarily obese hamsters: A possible manifestation of aging?

Borer

Bonna

Kielb

1988

Pharmacology Biochemistry and Behavior

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BORER, K. T., R. BONNA AND M. KIELB. Hippocampal serotonin mediates hypoactivity in dietarily obese hamsters:A possible manifestation of aging? PHARMACOL BIOCHEM BEHAV 31(4) [885][886][887][888][889][890][891][892] 1988.--To determine whether endogenous opiates mediate hyperactivity in food restricted hamsters and serotonergic fibers innervating the hippocampus mediate hypoactivity in obese hamsters, food restriction and high-fat diet supplementation were used to produce significant body fat changes (8 vs. 21%). The levels and pattern of spontaneous running were examined after IP saline or naloxone HC1 (20 mg/kg) and following the infusion of vehicle and 5,7-dihydroxytryptamine creatine sulfate (4/~g/2/zl) into rostromedial septum of mature female hamsters. Septum-medial preoptic area (POA), hippocampus, hypothalamus, and cortex were dissected from the three groups as well as from two additional groups of hamsters receiving vehicle or neurotoxin. Concentrations of serotonin, norepinephrine, and dopamine were measured in these tissues by HPLC method. Fat-fed hamsters were hypoactive relative to food-restricted hamsters. Naloxone had no significant effect on running behavior. Serotonin neurotoxin increased the running activity of fat-fed hamsters to the level displayed by control hamsters by increasing the number of runs, the total activity level, the speed of running and by decreasing the duration of pause:~. Neurotoxin led to selective deletion of serotonin in the hippocampus (77~) and parietal cortex (50%). Serotonergic fiber~ innervating the hippocampus thus appear to mediate the hypoactivity that is induced by dietary obesity iv. mature hamsters. Since serotonin mediates some other manifestations of aging, and slow weight increases characterize mid-portion of hamster life span, we hypothesize that serotonergic mediation of hypoactivity is another manifestation of aging. FastingHyperactivity Naloxone Limbic forebrain MECHANISMS which regulate body energy balance and control spontaneous running behavior are interrelated. This is apparent at the time of sexual maturation in rodents when there is a rapid increase in spontaneous running activity to an all-time high at the same time as the rate of somatic growth and of weight gain rapidly decline (8). It is also evident after the onset of sexual maturity, during the period of slow weight gain when activity levels decline in inverse proportion to increases in body size (4,8,37). Thus, when the weight of mature hamsters doubles, their spontaneous activity levels are reduced by about 50% (4,8). Furthermore, when accumulation of excess energy results in obesity, mice (45), rats (37,40), and hamsters (5) display even greater spontaneous hypoactivity.Reciprocal relationship between energy regulation and spontaneous running remains intact after some neurosurgical manipulations which affect both mechanisms. In the hamster, voluntary running levels are reduced by 80% following electrocoagulative lesions of rostromedial septum (10), horizontal transection of septo-hippocam...

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Increased Serum Growth Hormone and Somatic Growth in Adult Hamsters with Hippocampal Transections

Cited by 22 publications

References 45 publications

Hamster Prolactin: Physiological Changes in Blood and Pituitary Concentrations as Measured by a Homologous Radioimmunoassay

Hamster Prolactin: Physiological Changes in Blood and Pituitary Concentrations as Measured by a Homologous Radioimmunoassay

Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Hippocampal serotonin mediates hypoactivity in dietarily obese hamsters: A possible manifestation of aging?

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