Persistent Impairment of Insulin Secretory Response to Glucose in Adult Rats After Limited Period of Protein-Calorie Malnutrition Early in Life

Swenne, Ingemar; Crace, C. J.; Milner, R. D. G.

doi:10.2337/diab.36.4.454

Cited by 113 publications

(63 citation statements)

References 29 publications

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“…These results are corroborated by previous findings using similar approaches (Claeyssens et al, 1992;Ferreira et al, 2003;Heard, 1978;Heard et al, 1973;Swenne et al, 1987). Insulinaemia and glycaemia are unaltered in fasted LP rats compared to fasted NP rats, whereas in fed rats the insulinaemia is higher in NP than in LP rats and glycaemia remains unaltered (Latorraca et al, 1998;Reis et al, 1997).…”

Section: Discussionsupporting

confidence: 94%

“…Rats fed on diets containing a protein level comparable to that of undernourished humans have decreased glucose-induced insulin secretion, but increased insulin sensitivity in peripheral tissues (Escriva et al, 1991(Escriva et al, , 1992Swenne et al, 1987). Furthermore, islets isolated from undernourished rats show a significant decrease in the insulin secretory response to carbamylcholine (CCh) and phorbol 12-myristate 13-acetate (PMA) (Ferreira et al, 2003).…”

Section: Introductionmentioning

confidence: 98%

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Impaired insulin secretion and decreased expression of the nutritionally responsive ribosomal kinase protein S6K-1 in pancreatic islets from malnourished rats

et al. 2008

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 98%

Impaired insulin secretion and decreased expression of the nutritionally responsive ribosomal kinase protein S6K-1 in pancreatic islets from malnourished rats

et al. 2008

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“…This has been modelled in experimental rats by a maternal or early protein calorie malnutrition [12] and by maternal protein deficiency alone [13]. It was hypothesized that the impairment in insulin secretion may predispose a rat to the development of dia-I48 C. J. Petry et al…”

Section: Introductionmentioning

confidence: 99%

“…betes [12]. Subsequent studies in rats have modelled the findings in humans by showing that maternal protein restriction can lead to fetal growth retardation [13, 141, hypertension [14] and impaired glucose tolerance [15] in the offspring.…”

Section: Introductionmentioning

confidence: 99%

Early Protein Restriction and Obesity Independently Induce Hypertension in 1-Year-Old Rats

et al. 1997

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1. Recent studies have revealed a link between fetal and early post-natal, growth retardation and the development of features of the insulin resistance syndrome in later life. Obesity is also a strong risk factor for this syndrome. The aim of this study was to assess whether maternal and early protein restriction, which causes growth retardation, and obesity are risk factors that are independent for the development of certain features of the insulin resistance syndrome, especially hypertension. 2. Pregnant Sprague-Dawley rats were given either 20% or 8% protein isocaloric diets throughout pregnancy and lactation. Female offspring were weaned onto the same diets as their mothers and they remained on these diets until 70 days of age. Half the rats were then given standard laboratory chow, whilst the remainder were fed a highly palatable cafeteria-style diet. Rats were maintained on these diets for the remainder of the study. 3. Rats given the 8% protein diet remained physically lighter than comparable animals fed the 20% protein diet throughout the study. In contrast, cafeteria-fed rats showed excessive weight gain. At 1 year of age the rats had their systolic blood pressures and fasting lipids measured, as well as undergoing an intraperitoneal glucose-tolerance test. 4. Cafeteria-fed rats had worse glucose tolerances than controls and hypertriacylglycerolaemia. The early 8% protein rats had significantly increased blood pressures, as did the cafeteria-fed rats. These increases were additive, suggesting that early protein restriction, and later obesity, are indeed independent risk factors for the development of hypertension.

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“…Decreased insulin availability could also play a role in GH resistance during malnutrition, because low insulin concentrations are observed in protein-restricted rats (16) and in children with kwashiorkor (17). Also, insulin secretory responses to glucose and arginine are impaired in protein-caloric malnutrition (17)(18)(19), and decreased insulin correlates strongly with decreased IGF-I in diet-restricted animals (9) and children with kwashiorkor (17).…”

mentioning

confidence: 95%

Dietary Protein Restriction Decreases Insulin-Like Growth Factor I Independent of Insulin and Liver Growth Hormone Binding*

et al. 1989

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To determine the role of hypoinsulinemia and liver somatogenic (GH) receptors in growth retardation and decreased serum insulin-like growth factor I (IGF-I) levels during protein restriction, we have used a rat model where the effects of a low protein intake on body weight (BW), serum IGF-I concentration, and liver GH binding could be evaluated in the presence of low or high insulin concentrations. Two days after being made diabetic with streptozotocin (60 mg/kg BW), 6-week-old female rats (nine per group) were begun on a low (5%) or normal (15%) protein diet, without or with insulin supplementation (3 U lente daily). Nondiabetic rats fed both diets were used as controls (nine per group). In the nondiabetic animals, 7 days of protein restriction reduced BW gain by 50% (P less than 0.001), serum insulin by 44% (P less than 0.025), and serum IGF-I concentrations by 28% (P less than 0.001) without significantly changing liver GH binding. By day 9, BW was decreased in the diabetic animals by 12%, serum insulin by 80%, serum IGF-I by 55%, and liver GH binding by 62%; these effects were similar in the 5% and 15% protein-fed rats (P less than 0.001 vs. the corresponding controls). In the diabetes fed the normal diet, insulin treatment restored BW gain, serum IGF-I, and liver GH binding to normal values. In contrast, in the diabetics fed a protein-restricted diet and treated with insulin, BW gain and serum IGF-I concentrations remained low, similar to those in the malnourished controls. This diet-induced growth attenuation was observed despite high circulating insulin (2-3 times normal values), appropriate glucose control (63 +/- 9 mg/dl), and near restoration of liver GH binding. We conclude that while both protein restriction and diabetes attenuate growth and reduce IGF-I concentrations, the effects of protein restriction are independent of the effects of insulin and probably act by alteration of postreceptor mechanisms.

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Persistent Impairment of Insulin Secretory Response to Glucose in Adult Rats After Limited Period of Protein-Calorie Malnutrition Early in Life

Cited by 113 publications

References 29 publications

Impaired insulin secretion and decreased expression of the nutritionally responsive ribosomal kinase protein S6K-1 in pancreatic islets from malnourished rats

Impaired insulin secretion and decreased expression of the nutritionally responsive ribosomal kinase protein S6K-1 in pancreatic islets from malnourished rats

Early Protein Restriction and Obesity Independently Induce Hypertension in 1-Year-Old Rats

Dietary Protein Restriction Decreases Insulin-Like Growth Factor I Independent of Insulin and Liver Growth Hormone Binding*

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