scholarly journals Diabetes in Old Male Offspring of Rat Dams Fed a Reduced Protein Diet

2001 ◽  
Vol 2 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Clive J. Petry ◽  
Matthew W. Dorling ◽  
Dorota B. Pawlak ◽  
Susan E. Ozanne ◽  
C. Nicholas Hales

Restricted fetal growth is associated with increased risk for the future development of Type 2 diabetes in humans. The study aim was to assess the glucose tolerance of old (seventeen months) male rats, which were growth restricted in early life due to maternal protein restriction during gestation and lactation. Rat mothers were fed diets containing either 20% or 8% protein and all offspring weaned onto a standard rat diet. In old-age fasting plasma glucose concentrations were significantly higher in the low protein offspring: 8.4 (1.3)mmol/l v. 5.3 (1.3)mmol/l (p = 0.005), Areas under the curves were increased by 67% for glucose (p = 0.01) and 81% for insulin (p = 0.01) in these rats in intravenous glucose tolerance tests, suggesting (a degree of) insulin resistance. These results show that early growth retardation due to maternal protein restriction leads to the development of diabetes in old male rat offspring. The diabetes is predominantly associated with insulin resistance.

2019 ◽  
Vol 20 (3) ◽  
pp. 469 ◽  
Author(s):  
Marilia Martins Cavariani ◽  
Talita de Mello Santos ◽  
Dhrielly Natalia Pereira ◽  
Luiz Gustavo de Almeida Chuffa ◽  
Patricia Fernanda Felipe Pinheiro ◽  
...  

Background: Maternal protein restriction causes sperm alterations in the offspring, most of which are associated with epididymal functions. Because fluid reabsorption/secretion dynamics in the epididymal environment play important roles in the process of sperm maturation and concentration, we investigated the effects of maternal protein restriction on the expression of aquaporins (AQP1 and AQP9), vascular endothelial growth factor (VEGFa), and its receptor VEGFr-2 in different stages of postnatal epididymal development. Methods: Pregnant rats were divided into groups that received normoprotein (17% protein) and low-protein diets (6% protein) during gestation and lactation. After weaning, male rats only received the standard diet and were euthanized at the predetermined ages of 21, 44 and 120 days. Results: Maternal protein restriction decreased AQP1 and AQP9 expression in the initial segment and caput epididymis compared to the increased expression of these proteins observed in the corpus and cauda at all ages. Although protein restriction reduced the microvasculature density (MVD) on postnatal day (PND) 21 and 44, the MVD was unaltered on PND 120. Conclusions: Maternal protein restriction changed the structure or function of the offspring’s epididymis, specifically by affecting fluid dynamics and vasculogenesis in important stages of epididymis development.


2005 ◽  
Vol 289 (4) ◽  
pp. R1131-R1136 ◽  
Author(s):  
Lori L. Woods ◽  
Julie R. Ingelfinger ◽  
Ruth Rasch

Modest maternal dietary protein restriction in the rat leads to hypertension in adult male offspring. The purpose of this study was to determine whether female rats are resistant to developing the increased blood pressure seen in male rats after maternal protein restriction. Pregnant rats were fed a normal protein (19%, NP) or low-protein (8.5%, LP) diet throughout gestation. Renal renin protein and ANG II levels were reduced by 50–65% in male LP compared with NP pups, but were not suppressed in female LP compared with female NP. Mean arterial pressure in conscious, chronically instrumented adult female offspring (22 wk) was not different in LP (LP: 120 ± 3 mmHg vs. NP: 121 ± 2 mmHg), and glomerular filtration rate was also not different in LP vs. NP. The number of glomeruli per kidney was similar in adult LP and NP female offspring (LP: 26,050 ± 2,071 vs. NP: 26,248 ± 1,292, NP), and individual glomerular volume was also not different (LP: 0.92 ± 0.11 106μm3, LP vs. NP: 1.07 ± 0.11 106μm3); the total volume of all glomeruli per kidney was also not significantly different. Thus female rats are relatively resistant to the programming for adult hypertension by perinatal protein restriction that we have described in males. This resistance may be due to the fact that modest maternal protein restriction does not reduce the number of glomeruli with which females are endowed as it does in males. The intrarenal renin-angiotensin system during development may play a key role in this protective effect of female gender.


Author(s):  
Anwar Borai ◽  
Callum Livingstone ◽  
Gordon A A Ferns

Insulin resistance is a common condition, recognized to be a central feature of the metabolic syndrome, and strongly associated with an increased risk of cardiovascular disease and diabetes. The quantitative assessment of insulin sensitivity is not used for routine clinical purposes, but the emerging importance of insulin resistance has led to its wider application to research studies that have examined its pathogenesis, aetiology and consequences. The gold standard method for the determination of insulin sensitivity is the euglycaemic hyperinsulinaemic clamp from which indices of insulin sensitivity can be derived. The clamp technique is both expensive and complex to undertake and has prompted the use of surrogate methods, notably the insulin tolerance test and frequently sampled intravenous glucose tolerance test. Indices may be derived from these methods and correlate well with those derived from clamp studies. Indices can also be derived from measurements made during a standard oral glucose tolerance test and from one-off fasting specimens (e.g. homeostasis model assessment and quantitative insulin sensitivity check index). These indices lend themselves for use in large population studies where a relatively simple, inexpensive assessment is necessary. However, these tests all suffer from important limitations, including poor precision. Insulin resistance is increasingly being assessed in clinical situations, where relatively simple markers are required. Insulin-like growth factor binding protein-1 is an emerging marker which may be useful in this context.


2007 ◽  
Vol 293 (3) ◽  
pp. R1259-R1266 ◽  
Author(s):  
Jane L. Tarry-Adkins ◽  
Jaap A. Joles ◽  
Jian-Hua Chen ◽  
Malgorzata S. Martin-Gronert ◽  
Dionne M. van der Giezen ◽  
...  

Telomere shortening has been implicated in the aging process and various age-associated disorders, including renal disease. Moreover, oxidative stress has been identified as an initiator of accelerated telomere shortening. We have shown previously that maternal protein restriction during lactation leads to reduced renal telomere shortening, reduced albuminuria, and increased longevity in rats. Here we address the hypothesis that maternal protein restriction during lactation is nephroprotective and associated with increased expression of antioxidative enzymes and decreased age-dependent renal telomere shortening. Newborn rats were suckled by a dam fed either a control (20% protein) or low-protein (8% protein) diet. All animals were weaned onto standard chow. Offspring that had been suckled by protein-restricted mothers had reduced albuminuria, N-acetyl-glucosaminidase, and urinary aldosterone excretion. These animals also did not show significant age-dependent renal telomere shortening and hence had significantly longer telomeres at 12 mo of age. This lack of renal telomere shortening was associated with increased levels of the antioxidant enzymes manganese superoxide dismutase, glutathione peroxidase, and glutathione reductase. These findings suggest that beneficial effects of slow growth during lactation are associated with increased antioxidant capacity and prevention of age-dependent telomere shortening in the kidney.


1969 ◽  
Vol 45 (3) ◽  
pp. 375-386 ◽  
Author(s):  
C. R. C. HEARD ◽  
PAMELA A. J. HENRY

SUMMARY Dogs were fed diets of high, suboptimal or low protein value (NDpCal% = 10, 7 or 5) from weaning at approximately 6 weeks of age. Immunoreactive plasma insulin levels were measured during intravenous glucose tolerance tests at 8, 13 and 20 weeks of age. In the dogs fed on diets of suboptimal or low protein value, the assimilation coefficient (K) increased within the first 2 weeks on diet, without any corresponding increase in insulin output. Later, as glucose tolerance tended to become impaired, the insulin output increased significantly. A significant increase in insulin response also occurred in dogs fed the high protein diet, at approximately 6 months of age, when the growth rate had slowed down. The increase in insulin response to i.v. glucose, observed in dogs fed the diets of low protein value, did not occur in animals which became marasmic through loss of appetite. Such animals had a very feeble insulin response. The findings are discussed in relation to human protein-calorie deficiency syndromes (kwashiorkor and marasmus).


1992 ◽  
Vol 73 (4) ◽  
pp. 1227-1231 ◽  
Author(s):  
J. Bongbele ◽  
A. Gutierrez ◽  
S. Cardin ◽  
J. M. Lavoie

This study was undertaken to evaluate the effects of regular endurance-type exercise (i.e., swimming) on glucose tolerance and glucose-stimulated insulin response (GSIR) in 55- and 90-day-old peripubertal male rats. Intravenous glucose tolerance tests (0.5 g/kg) were done in four groups of male Sprague-Dawley rats: two groups of trained (TR; 55- and 90-day-old) and two groups of age- and weight-matched untrained (UNTR) rats. The UNTR rats were subjected to a continuous food restriction to maintain body weights equal to those of the TR rats. Rats were received in our laboratory after weaning at 21 days of age and were evaluated 48 h after the last exercise bout. No significant differences in body weights were found between TR and UNTR rats, at the age of either 55 or 90 days. A significant (P < 0.01) decrease in the mean integrated area under the glucose and insulin curves was observed in TR compared with UNTR groups in 55- as well as 90-day-old rats. These results indicate that exercise training in male rats improves the glucose tolerance and GSIR before and during puberty (21–90 days) independently of a reduction in body weight gain.


Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1103 ◽  
Author(s):  
Juhae Kim ◽  
Alee Choi ◽  
Young Hye Kwon

Maternal protein restriction is associated with increased risk of insulin resistance and inflammation in adulthood offspring. Here, we investigated whether maternal protein restriction could alter the risk of metabolic syndrome in postweaning high-fat (HF)-diet-challenged offspring, with focus on epididymal adipose tissue gene expression profile. Female ICR mice were fed a control (C) or a low-protein (LP) diet for two weeks before mating and throughout gestation and lactation, and their male offspring were fed an HF diet for 22 weeks (C/HF and LP/HF groups). A subset of offspring of control dams was fed a low-fat control diet (C/C group). In response to postweaning HF diet, serum insulin level and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased in control offspring. Maternal LP diet decreased HOMA-IR and adipose tissue inflammation, and increased serum adiponectin level in the HF-diet-challenged offspring. Accordingly, functional analysis revealed that differentially expressed genes (DEGs) enriched in cytokine production were downregulated in the LP/HF group compared to the C/HF group. We also observed the several annotated gene ontology terms associated with innate immunity and phagocytosis in down-regulated DEGs between LP/HF and C/C groups. In conclusion, maternal protein restriction alleviated insulin resistance and inflammation in young offspring mice fed a HF diet but may impair development of immune system in offspring.


2000 ◽  
Vol 279 (4) ◽  
pp. R1334-R1340 ◽  
Author(s):  
Jeffrey S. Thresher ◽  
Deborah A. Podolin ◽  
Yuren Wei ◽  
Robert S. Mazzeo ◽  
Michael J. Pagliassotti

The purpose of the present study was to determine whether fructose is the nutrient mediator of sucrose-induced insulin resistance and glucose intolerance. Toward this end, male rats were fed a purified starch diet (68% of total calories) for a 2-wk baseline period. After this, rats either remained on the starch (ST) diet or were switched to a sucrose (SU, 68% of total calories), fructose/glucose (F/G, 34/34% of total calories), or fructose/starch (F/ST, 34/34% of total calories) diet for 5 wk. Rats then underwent either an intravenous glucose tolerance test ( n = 10/diet) or a euglycemic, hyperinsulinemic clamp ( n = 8 or 9/diet). Incremental glucose and insulin areas under the curve in SU, F/G, and F/ST were on average 61 and 29% greater than ST, respectively, but not significantly different from one another. During clamps, glucose infusion rates (mg · kg−1 · min−1) required to maintain euglycemia were significantly lower ( P< 0.05) in SU, F/G, and F/ST (13.4 ± 0.9, 9.5 ± 1.7, 11.3 ± 1.3, respectively) compared with ST (22.8 ± 1.1). Insulin suppression of glucose appearance (mg · kg−1 · min−1) was significantly lower ( P < 0.05) in SU, F/G, and F/ST (5.6 ± 0.5, 2.2 ± 1.2, and 6.6 ± 0.7, respectively) compared with ST (9.6 ± 0.4). Insulin-stimulated glucose disappearance (mg · kg−1 · min−1) was significantly lower ( P < 0.05) in SU, F/G, and F/ST (17.9 ± 0.6, 16.2 ± 1.3, 15.3 ± 1.8, respectively) compared with ST (24.7 ± 1.2). These data suggest that fructose is the primary nutrient mediator of sucrose-induced insulin resistance and glucose intolerance.


1982 ◽  
Vol 35 (4) ◽  
pp. 381 ◽  
Author(s):  
M E Wastney ◽  
AC Arcus ◽  
CR Bickerstaffe ◽  
JE Wolff

Intravenous glucose tolerance tests were undertaken on fed twin-pregnant ewes at about 120 days of gestation by injecting 0�4 g glucose per kilogram of live weight, then measuring glucose and insulin concentrations in plasma over the next 2 h. An insulin resistance index was calculated from the product of Tl/2 for glucose disappearance and the plasma insulin concentrations integrated over time. Approximately 10 days later, the ewes were starved to induce ovine pregnancy toxaemia. During this period, the course of the hypoglycaemia and ketonaemia were followed by measuring metabolite concentrations in jugular blood samples obtained every 2-3 days. The existence of dehydration, acid-base imbalance and renal failure was also determined from packed cell volumes, serum CO2 content and serum concentrations of urea, creatinine and inorganic phosphate. Ewes that became recumbent and moribund with the disease were classified as susceptible whereas those asymptOl;natic after 10 days were classified as non-susceptible. Seven susceptible ewes had significantly higher insulin resistance indices (2043 � 670 s.d.) than did six non-susceptible ewes (1261 � 433 s.d.). It was concluded that poor control of glucose homeostasis may be an important predisposing factor in pathogenesis of the disease.


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