Reduced preabsorptive insulin response in aged rats: differential effects of amphetamine and arginine-vasopressin

Buwalda, Bauke; Strubbe, J.H.; Hoes, Madelien; Bohus, B.

doi:10.1016/0165-1838(91)90108-f

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…Hence, cephalic insulin contributes to a more stable plasma glucose, and its activation is a parasympathetic event (e. g., Strubbe & Steffens, 1993;Woods & Porte, 1974). As animals age, they develop parasympathetic dysfunction, and the consequent reduced cephalic insulin output may cause exaggerated postprandial insulin secretion and contribute to the pancreatic islet dysfunction in old age by exhausting the islets (e.g., see Buwalda, Strubbe, Hoes, & Bohus, 1991).…”

Section: Blood Glucosementioning

confidence: 99%

The psychobiology of meals

Woods

Strubbe

1994

Psychonomic Bulletin & Review

102

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Section: Blood Glucosementioning

confidence: 99%

The psychobiology of meals

Woods

Strubbe

1994

Psychonomic Bulletin & Review

102

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“…This may be caused by altered central parasympathetic drive. The phenomenon of attenuated vagal responses in combination with enhanced baseline parasympathetic activity was also seen in experiments with obese Wistar rats and very old (30 months) lean Wistar rats (9,28).…”

Section: Obesitymentioning

confidence: 78%

“…Since it is suggested that aging is accompanied with increased baseline parasympathetic activity leading to extinction of parasympathetic responses (9), it might be hypothesized that obese Zuckers, due to their continuously increased parasympathetic functioning, might display these typical characteristics of aging much earlier than normal rats. Alternatively or additionally, the absence of the preabsorptive insulin response and increased baseline insulin concentrations may be explained as a combined consequence of increased vagal activity at younger age and insulin insensitivity during the increase in fat mass during the late phase of obesity (11,12,19,21,49).…”

Section: Obesitymentioning

confidence: 99%

Energy Homeostasis, Autonomic Activity and Obesity

Scheurink¹,

Balkan²,

Nyakas³

et al. 1995

Obesity Research

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Obesity is often accompanied by alterations in both sympathetic and parasympathetic autonomic functions. The present paper summarizes the results of a number of studies designed to investigate autonomic functioning in normal, genetically, and experimentally obese rats. Particular emphasis is given to autonomic functioning and dysfunctioning in relation to the processes that are involved in the regulation of peripheral energy substrate homeostasis. It is concluded that alterations in autonomic regulation in obesity are determined by causal factors such as overeating, genetic make-up, age andfor the duration of obesity. 1995;3(S~ppl5):721S-727S.

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“…This EIR could be suppressed by prior administration of atropine or by subdiaphragmatic vagotomy, providing evidence for a parasympathetic origin of the EIR (11,46,50). Administration of atropine also attenuated and delayed the insulin response to intravenous or intragastric glucose loads (51), which indicates that the parasympathetic nervous system is also involved in the dynamics of insulin secretion during hyperglycemia.…”

Section: Energy Substrate Homeostasis and Autonomic Functioningmentioning

confidence: 99%

Overfeeding, autonomic regulation and metabolic consequences

Scheurink

Balkan

Strubbe

et al. 1996

Cardiovasc Drug Ther

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The autonomic nervous system plays an important role in the regulation of body processes in health and disease. Overfeeding and obesity (a disproportional increase of the fat mass of the body) are often accompanied by alterations in both sympathetic and parasympathetic autonomic functions. The overfeeding-induced changes in autonomic outflow occur with typical symptoms such as adiposity and hyperinsulinemia. There might be a causal relationship between autonomic disturbances and the consequences of overfeeding and obesity. Therefore studies were designed to investigate autonomic functioning in experimentally and genetically hyperphagic rats. Special emphasis was given to the processes that are involved in the regulation of peripheral energy substrate homeostasis. The data revealed that overfeeding is accompanied by increased parasympathetic outflow. Typical indices of vagal activity (such as the cephalic insulin release during food ingestion) were increased in all our rat models for hyperphagia. Overfeeding was also accompanied by increased sympathetic tone, reflected by enhanced baseline plasma norepinephrine (NE) levels in both VMH-lesioned animals and rats rendered obese by hyperalimentation. Plasma levels of NE during exercise were, however, reduced in these two groups of animals. This diminished increase in the exercise-induced NE outflow could be normalized by prior food deprivation. It was concluded from these experiments that overfeeding is associated with increased parasympathetic and sympathetic tone. In models for hyperphagia that display a continuously elevated nutrient intake such as the VMH-lesioned and the overfed rat, this increased sympathetic tone was accompanied by a diminished NE response to exercise. This attenuated outflow of NE was directly related to the size of the fat reserves, indicating that the feedback mechanism from the periphery to the central nervous system is altered in the overfed state.

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Reduced preabsorptive insulin response in aged rats: differential effects of amphetamine and arginine-vasopressin

Cited by 11 publications

References 24 publications

The psychobiology of meals

The psychobiology of meals

Energy Homeostasis, Autonomic Activity and Obesity

Overfeeding, autonomic regulation and metabolic consequences

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