Hepatic Glucose Production Oscillates in Synchrony with the Islet Secretory Cycle in Fasting Rhesus Monkeys

Goodner, Charles J.; Hom, F. G.; Koerker, Donna J.

doi:10.1126/science.7036347

Cited by 51 publications

(28 citation statements)

References 20 publications

(8 reference statements)

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“…Ultradian oscillations in insulinemia and glucagonemia with a period length of 70-140 min have been attributed to feedback mechanisms of glucose and seem to be entrained to the non-rapid eye movement (non-REM)/ REM sleep cycle (Kern et al 1996). More rapid oscillations of insulinemia, glucagonemia, and glycemia with a period of 5-15 min have been documented (Goodner et al 1977(Goodner et al , 1982Lang et al 1979Lang et al , 1982Weigle 1987;Jaspan et al 1986;Meier et al 2006;Menge et al 2011;Rohrer et al 2012). Different opinions have been expressed whether the pulsatile release of insulin and glucagon is a coupled or an independent process.…”

Section: Pulsatility Of Insulin Glucagon and Somatostatin Secretionmentioning

confidence: 97%

Physiological and Pathophysiological Control of Glucagon Secretion by Pancreatic α-Cells

Gilon¹,

Cheng-Xue²,

Lai³

et al. 2014

Islets of Langerhans

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Section: Pulsatility Of Insulin Glucagon and Somatostatin Secretionmentioning

confidence: 97%

Physiological and Pathophysiological Control of Glucagon Secretion by Pancreatic α-Cells

Gilon¹,

Cheng-Xue²,

Lai³

et al. 2014

Islets of Langerhans

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“…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].…”

mentioning

confidence: 99%

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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“…High-frequency insulin oscillations, normally an example of a regular hormonal rhythm (5,8,10,14,15,17,24,25,30), are disturbed in disease. Abnormalities in oscillations take a number of different forms, including loss of regularity, a decrease or increase in amplitude, or an alteration in frequency (1,9,12,16,19,20).…”

mentioning

confidence: 99%

Loss of entrainment of high-frequency plasma insulin oscillations in type 2 diabetes is likely a glucose-specific β-cell defect

Mao

Berman

Ipp

2004

American Journal of Physiology-Endocrinology and Metabolism

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. Loss of entrainment of high-frequency plasma insulin oscillations in type 2 diabetes is likely a glucose-specific ␤-cell defect. Am J Physiol Endocrinol Metab 287: E50 -E54, 2004. First published March 2, 2004 10.1152/ ajpendo.00555.2003.-Spontaneous high-frequency insulin oscillations are easily entrainable to exogenous glucose in vitro and in vivo, but this property is lost in type 2 diabetes (2-DM). We hypothesized that this lack of entrainment in 2-DM would be specific to glucose. This was tested in nine control and ten 2-DM subjects. Serial blood sampling at 1-min intervals was carried out for 60 min in the basal state and for 120 min while small (1-60 mg/kg) boluses of arginine were injected intravenously at exactly 29-min intervals. Samples were analyzed for insulin concentrations, and time series analysis was carried out using spectral analysis. In control subjects, the mean period of basal plasma insulin oscillations was 10.3 Ϯ 1.3 min and was entrained by arginine to a mean period of 14.9 Ϯ 0.6 min (P Ͻ 0.00001 vs. basal). Similarly, in 2-DM subjects, spontaneous insulin oscillations were entrained by arginine; mean basal insulin period was 10.0 Ϯ 1.0 min and 14.5 Ϯ 1.8 min with arginine boluses (P Ͻ 0.00001). All of the primary peaks observed in spectral analysis were statistically significant (P Ͻ 0.05). Percent total power of primary peaks ranged from 17 to 68%. Thus arginine boluses entrain spontaneous high-frequency insulin oscillations in 2-DM subjects. This represents a distinct and striking difference from the resistance of the ␤-cell to glucose entrainment in 2-DM. We conclude that loss of entrainment of spontaneous high-frequency insulin oscillations in 2-DM is likely a glucose-specific manifestation of ␤-cell secretory dysfunction.␤-cell dysfunction ABNORMALITIES IN PULSATILITY of hormone secretion have been implicated in secretory dysregulation in many endocrine systems (32). High-frequency insulin oscillations, normally an example of a regular hormonal rhythm (5,8,10,14,15,17,24,25,30), are disturbed in disease. Abnormalities in oscillations take a number of different forms, including loss of regularity, a decrease or increase in amplitude, or an alteration in frequency (1,9,12,16,19,20). It has also been suggested that a loss of regularity in high-frequency plasma insulin oscillations might represent an early secretory defect that can be demonstrated before the development of diabetes (2,21,27).Spontaneous high-frequency insulin oscillations are easily entrainable to an exogenous rhythm by small changes in glucose concentration in vitro (4). In vitro studies using isolated rat islets demonstrated spontaneous high-frequency insulin oscillations that were easily entrained to the rhythm of glucose pulses delivered at a different frequency (4). In vivo, high-frequency plasma insulin oscillations are also entrainable with exogenous glucose (18, 23). However, in type 2 diabetic (2-DM) patients, there is a complete loss of entrainment to glucose stimulation (11, 18). The present study was des...

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Hepatic Glucose Production Oscillates in Synchrony with the Islet Secretory Cycle in Fasting Rhesus Monkeys

Cited by 51 publications

References 20 publications

Physiological and Pathophysiological Control of Glucagon Secretion by Pancreatic α-Cells

Physiological and Pathophysiological Control of Glucagon Secretion by Pancreatic α-Cells

The in vivo regulation of pulsatile insulin secretion

Loss of entrainment of high-frequency plasma insulin oscillations in type 2 diabetes is likely a glucose-specific β-cell defect

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