Cephalic phase insulin release in normal weight males: verification and reliability

Teff, Karen L.; Mattes, Richard D.; Engelman, Karl

doi:10.1152/ajpendo.1991.261.4.e430

Cited by 83 publications

(103 citation statements)

References 24 publications

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“…Because Rodriguez-Diaz et al found sympathetic neurovascular contacts in human islets, they proceeded to emphasise species differences in innervation patterns. Our data, however, support species similarities in the innervation pattern: both mouse and human islets displayed a sympathetic neurovascular complex in the core, which is in line with the similar effect of autonomic activation on islet hormone release in animals and humans [3,10,[31][32][33][34].…”

Section: Discussionsupporting

confidence: 84%

3-D imaging and illustration of the perfusive mouse islet sympathetic innervation and its remodelling in injury

Chiu

Hua

et al. 2012

Diabetologia

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Aims/hypothesis Sympathetic nerves influence islet hormone levels in the circulation. Insights into islet sympathetic innervation and its remodelling in diabetes may impact future therapeutics. However, standard immunohistochemistry and microtome-based microscopy cannot provide an integral view of the islet neurovascular complex. We prepared transparent islet specimens to investigate the spatial relationship between sympathetic nerves, blood vessels and islet cells in normal, streptozotocin-injected and non-obese diabetic mouse models. Methods Cardiac perfusion of fluorescent lectin was used to label pancreatic blood vessels. Tyrosine hydroxylase and nuclear staining were used to reveal islet sympathetic innervation and microstructure. Optical clearing (i.e. use of immersion solution to reduce scattering) was applied to enable 3-dimensional confocal microscopy of islets to visualise the sympathetic neurovascular complex in space. Results Unlike previously reported morphology, we observed perfusive intra-islet, perivascular sympathetic innervation, in addition to peri-islet contacts of sympathetic nerves with alpha cells and sympathetic fibres encircling the adjacent arterioles. The intra-islet axons became markedly prominent in streptozotocin-injected mice (2 weeks after injection). In non-obese diabetic mice, lymphocytic infiltration remodelled the peri-islet sympathetic axons in early insulitis. Conclusions/interpretation We have established an imaging approach to reveal the spatial features of mouse islet sympathetic innervation. The neurovascular complex and sympathetic nerve-alpha cell contact suggest that sympathetic nerves modulate islet hormone secretion through blood vessels, in addition to acting directly on alpha cells. In islet injuries, sympathetic nerves undergo different remodelling in response to different pathophysiological cues.

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Section: Discussionsupporting

confidence: 84%

3-D imaging and illustration of the perfusive mouse islet sympathetic innervation and its remodelling in injury

Chiu

Hua

et al. 2012

Diabetologia

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“…A cephalic phase that is induced by sensory stimulation in the oral cavity and is involved in the regulation of insulin secretion after meal ingestion in humans has been demonstrated in several previous reports (3,5,(7)(8)(9)(10)33,34). Because atropine reduces the cephalic phase insulin release, it has been thought that cholinergic mechanisms may contribute (10).…”

Section: Discussionmentioning

confidence: 90%

“…he preabsorptive or cephalic phase insulin response, which lasts for ϳ10 min, is initiated by meal ingestion, as has been demonstrated in humans and rats (1)(2)(3)(4)(5)(6)(7)(8)(9). It is abolished by vagotomy in rats (1) and by atropine in rats (1) and humans (10), suggesting mediation by cholinergic mechanisms.…”

mentioning

confidence: 84%

The Cephalic Insulin Response to Meal Ingestion in Humans Is Dependent on Both Cholinergic and Noncholinergic Mechanisms and Is Important for Postprandial Glycemia

Åhrén

Holst²

2001

Diabetes

259

177

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We studied the mechanisms and physiological relevance of the cephalic insulin response to meal ingestion in 12 healthy women (age 63 ؎ 0.4 years; BMI 27.7 ؎ 1.7 kg/m 2 ). The ganglionic antagonist, trimethaphan, which impairs neurotransmission across parasympathetic and sympathetic autonomic ganglia, or atropine or saline was given intravenously during the first 15 min after ingestion of a standard meal (350 kcal). During saline infusion, insulin levels increased during the first 10 min after meal ingestion, whereas the first increase in glucose was evident at 15 min. The preabsorptive 10-min insulin response was reduced by 73 ؎ 11% by trimethaphan (P ‫؍‬ 0.009), accompanied by impaired reduction of glucose levels from 25 to 60 min after meal ingestion (⌬glucose ‫؍‬ -1.27 ؎ 0.5 [with saline] vs. 0.1 ؎ 0.4 mmol/l [with trimethaphan]; P ‫؍‬ 0.008). This reduction at 25-60 min in glucose levels correlated significantly to the 10-min insulin response (r ‫؍‬ 0.65, P ‫؍‬ 0.024). The 10-min insulin response to meal ingestion was also reduced by atropine, but only by 20 ؎ 9% (P ‫؍‬ 0.045), which was lower than the reduction with trimethaphan (P ‫؍‬ 0.004). The preabsorptive insulin response was not accompanied by any increase in circulating levels of gastric inhibitory polypeptide (GIP) or glucagon-like peptide 1 (GLP-1). In conclusion, 1) the early preabsorptive insulin response to meal ingestion in humans can be largely attributed to autonomic activation mediated by noncholinergic and cholinergic mechanisms, 2) this cephalic insulin response is required for a normal postprandial glucose tolerance, and 3) GIP and GLP-1 do not contribute to the preabsorptive cephalic phase insulin response to meal ingestion.

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“…For example, an initial pulse of insulin secretion in response to food ingestion occurs within ten minutes (peak value at 4 minutes post ingestion) in normal weight men, and this is before any change in blood glucose concentration due to absorption of nutrients could occur (Teff et al, 1991). The cephalic phase insulin response can also be triggered by non-nutritive sweet tasting substances, such as saccharin (Powley and Berthoud, 1985).…”

Section: Evidence For Cephalic Phase Responsesmentioning

confidence: 99%

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

2008

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Anticipatory physiological regulation is an adaptive strategy that enables animals to respond faster to physiologic and metabolic challenges. The cephalic phase responses are anticipatory responses that prepare animals to digest, absorb and metabolize nutrients. They enable the sensory aspects of the food to interact with the metabolic state of the animal to influence feeding behavior. The anticipatory digestive secretions and metabolic adjustments in response to food cues are key adaptations that affect digestive and metabolic efficiency and aid in controlling the resulting elevation of metabolic fuels in the blood. Cephalic phase responses enable digestion, metabolism and appetite to be regulated in a coordinated fashion. These responses have significant effects on meal size. For example, if the cephalic phase insulin response is blocked the result is poor glucose control and smaller meals. Cephalic phase responses also are linked to motivation to feed, and may play a more direct role in regulating meal size beyond the permissive one of ameliorating negative consequences of feeding. For example, the orexigenic peptide ghrelin appears to display a cephalic phase response, rising before expected meal times. This anticipatory ghrelin response increases appetite; interestingly it also enhances fat absorption, linking appetite with digestion and metabolism.

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Cephalic phase insulin release in normal weight males: verification and reliability

Cited by 83 publications

References 24 publications

3-D imaging and illustration of the perfusive mouse islet sympathetic innervation and its remodelling in injury

3-D imaging and illustration of the perfusive mouse islet sympathetic innervation and its remodelling in injury

The Cephalic Insulin Response to Meal Ingestion in Humans Is Dependent on Both Cholinergic and Noncholinergic Mechanisms and Is Important for Postprandial Glycemia

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

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