Pulsatile Insulin Release and Electrical Activity from Single ob/ob Mouse Islets of Langerhans

Rosário, Luı́s M.; Atwater, I; Scott, A. M.

doi:10.1007/978-1-4684-5314-0_40

Cited by 57 publications

(35 citation statements)

References 8 publications

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“…Similarly, studies on pancreas-transplanted subjects with shunts from the pancreas to the inferior caval vein, show increases in frequency versus healthy controls (8 versus 12 min per oscillation) [75]. Finally the reported frequency of 3 to 5 min per pulse in the isolated perifused islet [105,115,117,118] (10±17 min per pulse in [102,119,120]), suggests that there is a hierarchy of regulatory mechanisms with the fastest frequency in individual islets (3 to 5 min), followed by the perfused pancreas (6±10 min) and finally the in vivo insulin secretion (5 to 15 min). However, the open loop systems usually employed in in vitro rather than the closed loop system in vivo, with confounding effects of systemic dilution and hepatic insulin extraction, could cause a relatively low estimate of the in vivo pulse frequency.…”

Section: Contribution Of Pulsatile Insulin Release To the Overall Insmentioning

confidence: 91%

“…Examining data on in vitro insulin release at increasing glucose concentrations indicate increasing pulsatile release, whereas the basal release could be constant and glucose-unaffected [115,118]. The mechanism by which glucose stimulates insulin release seems to involve cyclic glycolysis [105,107], which generates oscillating intracellular concentrations of ATP [143], closure of ATP-dependent potassium channels and depolarization [120], increase in intracellular calcium [104,105,127], and subsequently an (ATP-dependent ?) exocytotic process.…”

Section: Metabolic Control Of In Vivo Pulsatile Insulin Secretionmentioning

confidence: 99%

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The in vivo regulation of pulsatile insulin secretion

2002

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In 1922, Karen Hansen [1] measured two series of blood glucose concentrations and reported oscillations in the peripheral concentrations of this substrate, results which were validated by simultaneous sampling from two sites to exclude the possibility that assay variability was a cause of the observed variations. Furthermore she studied the glucose concentrations in diabetic patients, and described both rapid and slower oscillations [1]. Half a century later the observation of rapid oscillations was shown to correlate with oscillations in the peripheral insulin concentrations [2±6], with glucose concentration increases slightly out of phase with insulin secretion pulses [7]. The pulsatile secretion of insulin was shown to coincide with islet pulsatile release of glucagon [4,6,8,9], and somatostatin [9±11]. A number of studies have reported importance of this release pattern for optimal insulin action [10, 12±21, 21±25], for overall insulin secretion [26±35], and for possible development of disease [36±43]. Studies on pulsatile insulin secretion could therefore be important for appreciating how insulin release is regulated overall and how Diabetologia (2002) 45: 3±20 ReviewsThe in vivo regulation of pulsatile insulin secretion

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Section: Contribution Of Pulsatile Insulin Release To the Overall Insmentioning

confidence: 91%

Section: Metabolic Control Of In Vivo Pulsatile Insulin Secretionmentioning

confidence: 99%

The in vivo regulation of pulsatile insulin secretion

2002

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“…Oscillations in the ␤-cell membrane potential, cytoplasmic Ca 2ϩ concentration ([Ca 2ϩ ] i ), and metabolism, with similar frequencies as the plasma insulin oscillations, have been described and suggested to be responsible for the pulsatile release of insulin (11)(12)(13)(14)(15)(16)(17)(18)(19). However, observations and conclusions made from experiments with isolated ␤-cells or islets do not necessarily translate into the in vivo situation.…”

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confidence: 82%

Role of Oscillations in Membrane Potential, Cytoplasmic Ca2+, and Metabolism for Plasma Insulin Oscillations

Bergsten

2002

Diabetes

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(1,2). The frequency of the insulin pulses is important for the action of the hormone. Significantly less insulin is required when administered in a pulsatile fashion rather than as a bolus injection (3-7), which may result in different expression of the insulin receptor on target tissue (8). Indeed, a contributing cause to the glucose intolerance in type 2 diabetes may be related to the loss of the regular accentuated plasma insulin oscillations (9,10), which could aggravate insulin resistance by receptor downregulation.The oscillatory behavior seems to be intrinsic of the ␤-cell. Oscillations in the ␤-cell membrane potential, cytoplasmic Ca 2ϩ concentration ([Ca 2ϩ ] i ), and metabolism, with similar frequencies as the plasma insulin oscillations, have been described and suggested to be responsible for the pulsatile release of insulin (11-19). However, observations and conclusions made from experiments with isolated ␤-cells or islets do not necessarily translate into the in vivo situation. When evaluating the possible effects of oscillatory membrane potential, [Ca 2ϩ ] i , and metabolism on plasma insulin oscillations, oscillatory activities with different frequencies have to be considered. In this context, the oscillatory activity with a frequency of 2-7 oscillations (osc) per minute and that with a frequency of 0.2-0.4 osc/min will be discussed. Experimental observations of these rapid and slow islet oscillatory activities in vivo and in vitro are reviewed, together with an in vivo model of the ␤-cell, where the role of the oscillatory activities in membrane potential, [Ca 2ϩ ] i , and metabolism for the generation of plasma insulin oscillations are presented and discussed. IN VITRO OSCILLATIONS OF ISLET MEMBRANE POTENTIAL AND [Ca 2؉ ] iRapid oscillations in membrane potential and [Ca 2ϩ ] i (2-7 osc/min) have been observed and characterized in the isolated islet (14,15,20 -29). The membrane potential measurements consist of "slow waves," which are periods of depolarization when accumulations of action potentials ("bursts") promote influx of Ca 2ϩ , interspersed with periods of hyperpolarization, when no Ca 2ϩ influx is present. These slow waves give rise to the rapid oscillations in [Ca 2ϩ ] i . The glucose concentration affects both the duration of the bursts and the time relationship between periods of depolarization and hyperpolarization, i.e., the frequency of the slow waves (30).Slow oscillations (0.2-0.4 osc/min) in [Ca 2ϩ ] i (15,23,26 -28,31) and in membrane potential activity (32-34) have been recorded and characterized in the isolated islet. The frequency of these oscillations is not affected by the glucose concentration (23,27). The slow oscillations of [Ca 2ϩ ] i are primarily observed in cultured islets. As the culture period is extended, the rapid [Ca 2ϩ ] i oscillations disappear in favor of the slow ones, which also disappear after prolonged culture (31). The glucose concentration during culture is also decisive for the [Ca 2ϩ ] i oscillatory pattern (26). Although a low...

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“…Finally, the reported frequency of 3-5 min per pulse in the isolated perifused islet (68,97,108 -110) (10 -17 min per pulse in refs. 94,111,112) suggests that there is a hierarchy of regulatory mechanisms with the fastest frequency in individual islets (3-5 min), followed by the perfused pancreas (6 -10 min), and finally the in vivo insulin secretion (5-15 min). Studies comparing sampling intensities, sampling sites, and mathematical strategies for the detection of insulin secretory bursts suggest that studies sampling every 2 min may underestimate the frequency, and that analysis of data based on pulses limited by a significant increase and decrease in insulin concentrations in the peripheral circulation will underestimate the frequency of insulin secretory bursts when secretory bursts tend to overlap (15,21,26,69,72).…”

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confidence: 99%

Pulsatile Insulin Secretion: Detection, Regulation, and Role in Diabetes

et al. 2002

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Insulin concentrations oscillate at a periodicity of 5-15 min per oscillation. These oscillations are due to coordinate insulin secretory bursts, from millions of islets. The generation of common secretory bursts requires strong within-islet and within-pancreas coordination to synchronize the secretory activity from the ␤-cell population. The overall contribution of this pulsatile mechanism dominates and accounts for the majority of insulin release. This review discusses the methods involved in the detection and quantification of periodicities and individual secretory bursts. The mechanism by which overall insulin secretion is regulated through changes in the pulsatile component is discussed for nerves, metabolites, hormones, and drugs. The impaired pulsatile secretion of insulin in type 2 diabetes has resulted in much focus on the impact of the insulin delivery pattern on insulin action, and improved action from oscillatory insulin exposure is demonstrated on liver, muscle, and adipose tissues. Therefore, not only is the dominant regulation of insulin through changes in secretory burst mass and amplitude, but the changes may affect insulin action. Finally, the role of impaired pulsatile release in early type 2 diabetes suggests a predictive value of studies on insulin pulsatility in the development of this disease. Diabetes 51 (Suppl. 1): S245-S254, 2002

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Pulsatile Insulin Release and Electrical Activity from Single ob/ob Mouse Islets of Langerhans

Cited by 57 publications

References 8 publications

The in vivo regulation of pulsatile insulin secretion

The in vivo regulation of pulsatile insulin secretion

Role of Oscillations in Membrane Potential, Cytoplasmic Ca2+, and Metabolism for Plasma Insulin Oscillations

Pulsatile Insulin Secretion: Detection, Regulation, and Role in Diabetes

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