Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

León–Quinto, Trinidad; Adnot, P.; Portha, Bernard

doi:10.1007/s001250050784

Cited by 15 publications

(12 citation statements)

References 44 publications

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“…In the present work, we described in malnourished animals an impaired glucose regulation of both ␣-cell Ca 2ϩ signaling, an essential step in exocytosis, and glucagon secretion. However, to the best of our knowledge, there are no specific studies describing the ␣-cell behavior during protein-deficient states, several works in malnourished rats have reported increased plasma glucagon levels and have suggested an altered ␣-cell function (18,41). Here, we confirm that pancreatic ␣-cells present an altered regulation.…”

Section: Discussionsupporting

confidence: 89%

“…These studies in rats indicated a lower hepatic response to glucagon and/or liver function deregulation in malnourished animals. Additionally, increased plasma glucagon levels have been also observed in chronic malnutrition (18). Although the majority of these previous reports have only focused on glucagon action on hepatic glucose handling, in our current work, we additionally reported 1) adaptations of glucose-regulated Ca 2ϩ signaling and glucagon secretion at the cellular level, 2) alterations in ␣-cell mass, and 3) changes in glucagon action and fasting responses at the molecular level in receptor and postreceptor steps.…”

Section: Discussionmentioning

confidence: 67%

“…Despite the importance of glucagon on glucose homeostasis, the vast majority of the above-mentioned studies are focused only on ␤-cells. Additionally, few studies show altered plasma glucagon levels in human and animals during malnutrition, pointing to altered ␣-cell function in these conditions (17)(18)(19). Thus, in the present study, we have analyzed the structural and functional adaptations of the pancreatic ␣-cell as well as changes in glucagon action on liver in a mouse model of protein malnutrition.…”

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confidence: 90%

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Functional and Structural Adaptations in the Pancreatic α-Cell and Changes in Glucagon Signaling During Protein Malnutrition

et al. 2012

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Chronic malnutrition leads to multiple changes in β-cell function and peripheral insulin actions to adapt glucose homeostasis to these restricted conditions. However, despite glucose homeostasis also depends on glucagon effects, the role of α-cells in malnutrition is largely unknown. Here, we studied α-cell function and hepatic glucagon signaling in mice fed with low-protein (LP) or normal-protein diet for 8 wk after weaning. Using confocal microscopy, we found that inhibition of Ca²⁺ signaling by glucose was impaired in α-cells of LP mice. Consistent with these findings, the ability of glucose to inhibit glucagon release in isolated islets was also diminished in LP mice. This altered secretion was not related with changes in either glucagon gene expression or glucagon content. A morphometric analysis showed that α-cell mass was significantly increased in malnourished animals, aspect that was probably related with their enhanced plasma glucagon levels. When we analyzed the hepatic function, we observed that the phosphorylation of protein kinase A and cAMP response-binding element protein in response to fasting or exogenous glucagon was impaired in LP mice. Additionally, the up-regulated gene expression in response to fasting observed in the hepatic glucagon receptor as well as several key hepatic enzymes, such as peroxisome proliferator-activated receptor γ, glucose-6-phosphatase, and phosphoenolpyruvate carboxykinase, was altered in malnourished animals. Finally, liver glycogen mobilization in response to fasting and the ability of exogenous glucagon to raise plasma glucose levels were lower in LP mice. Therefore, chronic protein malnutrition leads to several alterations in both the α-cell function and hepatic glucagon signaling.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 67%

mentioning

confidence: 90%

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Functional and Structural Adaptations in the Pancreatic α-Cell and Changes in Glucagon Signaling During Protein Malnutrition

et al. 2012

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“…Persistent alterations of the autonomous nervous system may also be supposed. Some studies indeed demonstrated a long-term impact of protein malnutrition on the reactivity of the sympathetic system (21,24).…”

Section: Discussionmentioning

confidence: 99%

Development of β-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy

Bertin

Gangnerau

Bellon

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. Development of ␤-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy. Am J Physiol Regul Integr Comp Physiol 283: R623-R630, 2002. First published May 16, 2002 10.1152 10. / ajpregu.00037.2002 malnutrition is now proposed as a risk factor of later obesity and type II diabetes. We previously analyzed the long-term impact of reduced protein and/or energy intake strictly limited to the last week of pregnancy in Wistar rats. Three protocols of gestational malnutrition were used: 1) low-protein isocaloric diet (5 instead of 15%) with pair feeding to the mothers receiving the control diet, 2) restricted diet (50% of control diet), and 3) low protein-restricted diet (50% of low-protein diet). Only isolated protein restriction induced a long-term ␤-cell mass decrease. In the present study, we used the same protocols of food restriction to analyze their short-term impact (on day 21.5 of pregnancy) on ␤-cell mass development. A 50% ␤-cell mass decrease was present in the three restricted groups, but low-protein diet, either associated or not to energy restriction, increased fetal ␤-cell insulin content. Among all the parameters analyzed to further explain our results, we found that the fetal plasma level of taurine was lowered by lowprotein diet and was the main predictor of the fetal plasma insulin level (r ϭ 0.63, P Ͻ 0.01). In conclusion, rat fetuses exposed to protein and/or energy restriction during the third part of pregnancy have a similar dramatic decrease in ␤-cell mass, and their ability to recover ␤-cell mass development retardation depends on the type of malnutrition used. Moreover, our results support the hypothesis that taurine might play an important role in fetal ␤-cell mass function. endocrine pancreas EPIDEMIOLOGICAL DATA IN VARIOUS human populations show that low birth weight and especially thinness at birth are associated with susceptibility to the development of impaired glucose tolerance/type II diabetes in adult life (16,23,26,28,31,32). This association has been interpreted as reflecting long-term effects of nutritional factors that reduce fetal growth and impair the development of tissues regulating glucose metabolism (14,29,36).Among these tissues, the endocrine pancreas, and especially ␤-cells, could suffer from fetal malnutrition. Babies with intrauterine growth retardation have a marked reduction in the size of their endocrine pancreas (41). Animal studies also report that fetal malnutrition is associated with persistently impaired pancreatic ␤-cell function and development (11,13). With the use of a low-protein diet during whole rat pregnancy, reduced proliferation rate, size, and insulin content of pancreas islets were observed in fetuses at the end of pregnancy (11,38).However, human data did not highlight a clear relationship between body weight or ponderal index (weight/height 3 ) at birth and ␤-cell function in adult age (8), and human fetal malnutrition was reported to be more strongly related to insulin resistance (5,9,10,23,26,31,40). Some...

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“…Despite elevation of energy expenditure, body fat content increases (13,16), possibly due to positive adaptation that allows part of the excess carbohydrate ingested relative to protein to be stored as lipid (14). The increased sympathetic nervous system activity appears to contribute partly to decreased glucose-stimulated insulin secretion (17), which is compensated by enhanced glucose tolerance and insulin action seen in protein restriction (18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

Macedo

Ferreira

Menegaz

et al. 2008

Braz J Med Biol Res

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During pregnancy and protein restriction, changes in serum insulin and leptin levels, food intake and several metabolic parameters normally result in enhanced adiposity. We evaluated serum leptin and insulin levels and their correlations with some predictive obesity variables in Wistar rats (90 days), up to the 14th day of pregnancy: control non-pregnant (N = 5) and pregnant (N = 7) groups (control diet: 17% protein), and low-protein non-pregnant (N = 5) and pregnant (N = 6) groups (low-protein diet: 6%). Independent of the protein content of the diet, pregnancy increased total (F 1,19 = 22.28, P < 0.001) and relative (F 1,19 = 5.57, P < 0.03) food intake, the variation of weight (F 1,19 = 49.79, P < 0.000) and final body weight (F 1,19 = 19.52, P < 0.001), but glycemia (F 1,19 = 9.02, P = 0.01) and the relative weight of gonadal adipose tissue (F 1,19 = 17.11, P < 0.001) were decreased. Pregnancy (F 1,19 = 18.13, P < 0.001) and low-protein diet (F 1,19 = 20.35, P < 0.001) increased the absolute weight of brown adipose tissue. However, the relative weight of this tissue was increased only by protein restriction (F 1,19 = 15.20, P < 0.001) and the relative lipid in carcass was decreased in low-protein groups (F 1,19 = 4.34, P = 0.05). Serum insulin and leptin levels were similar among groups and did not correlate with food intake. However, there was a positive relationship between serum insulin levels and carcass fat depots in low-protein groups (r = 0.37, P < 0.05), while in pregnancy serum leptin correlated with weight of gonadal (r = 0.39, P < 0.02) and retroperitoneal (r = 0.41, P < 0.01) adipose tissues. Unexpectedly, protein restriction during 14 days of pregnancy did not alter the serum profile of adiposity signals and their effects on food intake and adiposity, probably due to the short term of exposure to low-protein diet.

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Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

Cited by 15 publications

References 44 publications

Functional and Structural Adaptations in the Pancreatic α-Cell and Changes in Glucagon Signaling During Protein Malnutrition

Functional and Structural Adaptations in the Pancreatic α-Cell and Changes in Glucagon Signaling During Protein Malnutrition

Development of β-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy

Correlation of serum leptin and insulin levels of pregnant protein-restricted rats with predictive obesity variables

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