Evidence for decreased sensitivity to glucose of isolated islets from spiny mice (Acomys cahirinus)

Gutzeit, A.; Rabinovitch, Alex; Karakash, C.; Stauffacher, Werner; Renold, Albert E.; Cerasi, Erol

doi:10.1007/bf01222001

Cited by 19 publications

(22 citation statements)

References 22 publications

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“…Furthermore, even when this is adhered to, differences noted between species must be interpreted cautiously: what is 'normal' for one species may not be normal for another. With these restrictions in mind, studies have been performed on proinsulin synthesis in islets of Langerhans from Acomys cahirinus, the spiny mouse, in which insulin release is markedly insensitive to glucose, when compared with other rodents such as rats or mice [6][7][8][9].…”

Section: Discussionmentioning

confidence: 99%

“…These differences in the response profile to glucose have been detected in vivo, after either intraperitoneal [4][5] or intravenous [6] glucose injection, and in vitro, using isolated islets [7][8][9]. While acomys islets respond slowly to glucose, the total release of insulin over a two hour period may be comparable to that of rats, at least at higher glucose concentrations [7][8][9], suggesting predominantly early decreased sensitivity to glucose. Indeed, when the early and late release phases were compared in some detail [7][8][9], it was confirmed that the early phase (1-10 rain) of insulin release from acomys islets exhibited both decreased sensitivity to glucose and a decreased release capacity.…”

mentioning

confidence: 99%

“…Acomys cahirinus maintained in the Geneva colony exhibit hyperplasia of the islets of Langerhans [1][2][3] and a retarded as well as reduced rate of insulin release in response to glucose challenge by comparison with rats or mice [4][5][6][7]. These differences in the response profile to glucose have been detected in vivo, after either intraperitoneal [4][5] or intravenous [6] glucose injection, and in vitro, using isolated islets [7][8][9]. While acomys islets respond slowly to glucose, the total release of insulin over a two hour period may be comparable to that of rats, at least at higher glucose concentrations [7][8][9], suggesting predominantly early decreased sensitivity to glucose.…”

mentioning

confidence: 99%

“…The results demonstrate a decreased responsiveness of proinsulin synthesis to glucose in acomys and are discussed in terms of the known decreased sensitivity of insulin release in this animal. Acomys cahirinus maintained in the Geneva colony exhibit hyperplasia of the islets of Langerhans [1][2][3] and a retarded as well as reduced rate of insulin release in response to glucose challenge by comparison with rats or mice [4][5][6][7]. These differences in the response profile to glucose have been detected in vivo, after either intraperitoneal [4][5] or intravenous [6] glucose injection, and in vitro, using isolated islets [7][8][9].…”

mentioning

confidence: 99%

“…While acomys islets respond slowly to glucose, the total release of insulin over a two hour period may be comparable to that of rats, at least at higher glucose concentrations [7][8][9], suggesting predominantly early decreased sensitivity to glucose. Indeed, when the early and late release phases were compared in some detail [7][8][9], it was confirmed that the early phase (1-10 rain) of insulin release from acomys islets exhibited both decreased sensitivity to glucose and a decreased release capacity. By contrast, the late phase (20-30 rain) of insulin release from acomys islets exhibited only decreased sensitivity to glucose.…”

mentioning

confidence: 99%

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Proinsulin synthesis in islets of Langerhans from spiny mice (Acomys cahirinus). comparison with rats and mice

et al. 1976

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Summary. Proinsulin synthesis in response tO different concentrations of glucose has been studied in islets of Langerhans of acomys, rat and mouse. The response to increased glucose was small in acomys when compared with rat or mouse. The time course of the effect of glucose on proinsulin synthesis was also studied in sequential 15 min periods up to 60 min. With 5.5 mM glucose the rate of 3H-leucine incorporation for acomys islets was greater over the periods 15-30, 30-45 and 45-60 min after the addition of glucose to the islets than at 0-15 rain. By contrast rat islets exhibited a greater glucose-induced stimulation between 15-30 and 30-45 min relative to the 0-15 min period and a further increase of the incorporation rate between 45 and 60 min. With 27.5 mM glucose acceleration of incorporation relative to the first 15 min period occurred at 15-30 min; it was then stable up to 60 min for islets both from acomys and from rat. Incorporation into total protein was much greater in acomys than in rat or mouse: thus in 2.75 mM glucose, acomys islets incorporated 5 and 19 times more 3H-leucine into total protein than did islets from rat or mouse respectively. In 27.5 mM glucose the incorporation into total protein of the islets from acomys was 4 and 13 times greater. Islet content of insulin was similar for all three species. No significant changes in ATP content were observed in response to changes in glucose concentration from 2.75 to 27.5 mM. The results demonstrate a decreased responsiveness of proinsulin synthesis to glucose in acomys and are discussed in terms of the known decreased sensitivity of insulin release in this animal. Acomys cahirinus maintained in the Geneva colony exhibit hyperplasia of the islets of Langerhans [1][2][3] and a retarded as well as reduced rate of insulin release in response to glucose challenge by comparison with rats or mice [4][5][6][7]. These differences in the response profile to glucose have been detected in vivo, after either intraperitoneal [4][5] or intravenous [6] glucose injection, and in vitro, using isolated islets [7][8][9]. While acomys islets respond slowly to glucose, the total release of insulin over a two hour period may be comparable to that of rats, at least at higher glucose concentrations [7][8][9], suggesting predominantly early decreased sensitivity to glucose. Indeed, when the early and late release phases were compared in some detail [7][8][9], it was confirmed that the early phase (1-10 rain) of insulin release from acomys islets exhibited both decreased sensitivity to glucose and a decreased release capacity. By contrast, the late phase (20-30 rain) of insulin release from acomys islets exhibited only decreased sensitivity to glucose. As these time/secretion characteristics resemble in some respects observations reported in latent diabetes as well as maturity onset diabetes in man [10][11][12] acomys has attracted attention as a possible "model" of potential usefulness. Because of this and because the insensitivity to glucose might be carried over to the ...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Proinsulin synthesis in islets of Langerhans from spiny mice (Acomys cahirinus). comparison with rats and mice

et al. 1976

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Overnutrition in spiny mice (Acomys cahirinus): ?-cell expansion leading to rupture and overt diabetes on fat-rich diet and protective energy-wasting elevation in thyroid hormone on sucrose-rich diet

Shafrir

2000

Diabetes Metab. Res. Rev.

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Previous studies The investigation of diabetes propensity in spiny mice, performed in Geneva and Jerusalem colonies, is reviewed. Spiny mice live in semi‐desert regions of the eastern Mediterranean countries. Those transferred to Geneva in the 1950s were maintained on a rodent diet supplemented by fat‐rich seeds. They became obese, exhibited pancreatic islet hyperplasia and hypertrophy. Low insulin secretion response was characteristic of this species, despite ample pancreatic content of insulin. After a few months, diabetes with ketosis occurred, often suddenly, in association with islet cell disintegration. In Jerusalem the spiny mice were collected from their native habitat and placed on diets containing 50% sucrose or fat‐rich seed diets. On a sucrose‐rich diet, spiny mice developed hepatomegaly, lipogenic enzyme hyperactivity, and elevation in very low density lipoproteins as a result of metabolism of the fructose component mainly in the liver. No overt diabetes or pancreatic islet disintegration were observed, although insulin content and β‐cell hypertrophy and hyperplasia were apparent. On a fat‐rich diet, spiny mice exhibited marked weight gain, adipose tissue growth and low hepatic lipogenesis. The obesity was accompanied by mild hyperglycemia and hyperinsulinemia with glucose intolerance leading to an occasional glucosuria after several months on the diet. Novel experiments The sucrose diet induced an extrathyroidal elevation of triiodothyronine (T3). Serum T3 level and hepatic T4–T3 conversion were increased, while serum T4 levels tended to decrease. The activity of the T3‐inducible hepatic mitochondrial FAD‐glycerophosphate oxidase and K+/Na+‐ATPase, as well as body temperature were increased, indicating that the sucrose diet was associated with enhanced thermogenesis and energy‐wasting metabolic cycling. The sucrose‐rich diet might exert an adaptive thermogenesis‐mediated defense mechanism, protecting against excessive weight gain and disruptive pancreatic islet lesion. After 18 months maintenance on sucrose‐rich versus fat‐rich diets the number of animals surviving was significantly higher on the sucrose diet whereas on the fat diet a significant number of animals succumbed to expansive islet cell disruption and diabetes. Copyright © 2000 John Wiley & Sons, Ltd.

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Hereditary Hyperglycemic Syndromes in Laboratory Rodents

Stauffacher¹,

Kikkawa²,

Amherdt³

et al. 1976

The Genetics of Diabetes Mellitus

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Evidence for decreased sensitivity to glucose of isolated islets from spiny mice (Acomys cahirinus)

Cited by 19 publications

References 22 publications

Proinsulin synthesis in islets of Langerhans from spiny mice (Acomys cahirinus). comparison with rats and mice

Proinsulin synthesis in islets of Langerhans from spiny mice (Acomys cahirinus). comparison with rats and mice

Overnutrition in spiny mice (Acomys cahirinus): ?-cell expansion leading to rupture and overt diabetes on fat-rich diet and protective energy-wasting elevation in thyroid hormone on sucrose-rich diet

Hereditary Hyperglycemic Syndromes in Laboratory Rodents

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