Effect of catch-up growth after food restriction on the entero-insular axis in rats

Chen, Lulu; Yang, Wei; Zheng, Juan; Hu, Xiang; Kong, Wen; Zhang, Haohao

doi:10.1186/1743-7075-7-45

Cited by 15 publications

(14 citation statements)

References 39 publications

(39 reference statements)

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“…Other studies have suggested that the β-cell proportional area (relative to total cellular area) and islet number was decreased in rats undergoing nutrient restriction for a period of 4 weeks when compared with a control group fed for ad libitum intake (Chen et al, 2010). Our results suggested no effect of global nutrient restriction on insulinpositive area (relative to section of tissue) in ewes.…”

Section: Discussioncontrasting

confidence: 47%

Influence of nutrient restriction and melatonin supplementation of pregnant ewes on maternal and fetal pancreatic digestive enzymes and insulin-containing clusters

Keomanivong

Lemley

Camacho

et al. 2016

Animal

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Primiparous ewes ( n = 32) were assigned to dietary treatments in a 2 × 2 factorial arrangement to determine effects of nutrient restriction and melatonin supplementation on maternal and fetal pancreatic weight, digestive enzyme activity, concentration of insulin-containing clusters and plasma insulin concentrations. Treatments consisted of nutrient intake with 60% (RES) or 100% (ADQ) of requirements and melatonin supplementation at 0 (CON) or 5 mg/day (MEL). Treatments began on day 50 of gestation and continued until day 130. On day 130, blood was collected under general anesthesia from the uterine artery, uterine vein, umbilical artery and umbilical vein for plasma insulin analysis. Ewes were then euthanized and the pancreas removed from the ewe and fetus, trimmed of mesentery and fat, weighed and snap-frozen until enzyme analysis. In addition, samples of pancreatic tissue were fixed in 10% formalin solution for histological examination including quantitative characterization of size and distribution of insulin-containing cell clusters. Nutrient restriction decreased ( P ⩽ 0.001) maternal pancreatic mass (g) and α-amylase activity (U/g, kU/pancreas, U/kg BW). Ewes supplemented with melatonin had increased pancreatic mass ( P = 0.03) and α-amylase content (kU/pancreas and U/kg BW). Melatonin supplementation decreased ( P = 0.002) maternal pancreatic insulin-positive tissue area (relative to section of tissue), and size of the largest insulin-containing cell cluster ( P = 0.04). Nutrient restriction decreased pancreatic insulin-positive tissue area ( P = 0.03) and percent of large (32 001 to 512 000 µm 2 ) and giant (⩾512 001 µm 2 ) insulin-containing cell clusters ( P = 0.04) in the fetus. Insulin concentrations in plasma from the uterine vein, umbilical artery and umbilical vein were greater ( P ⩽ 0.01) in animals receiving 100% requirements. When comparing ewes to fetuses, ewes had a greater percentage of medium insulin-containing cell clusters (2001 to 32 000 µm 2 ) while fetuses had more ( P < 0.001) pancreatic insulin-positive area (relative to section of tissue) and a greater percent of small, large and giant insulin-containing cell clusters ( P ⩽ 0.02). Larger insulin-containing clusters were observed in fetuses ( P < 0.001) compared with ewes. In summary, the maternal pancreas responded to nutrient restriction by decreasing pancreatic weight and activity of digestive enzymes while melatonin supplementation increased α-amylase content. Nutrient restriction decreased the number of pancreatic insulin-containing clusters in fetuses while melatonin supplementation did not influence insulin concentration. This indicated using melatonin as a therapeutic agent to mitigate reduced pancreatic function in the fetus due to maternal nutrient restriction may not be beneficial.Keywords: development, ewes, melatonin, nutrient restriction, pancreas ImplicationsMelatonin is a potential therapeutic to overcome negative effects of nutrient restriction during pregnancy because of its roles in regulating blood flow and gastr...

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Section: Discussioncontrasting

confidence: 47%

Influence of nutrient restriction and melatonin supplementation of pregnant ewes on maternal and fetal pancreatic digestive enzymes and insulin-containing clusters

Keomanivong

Lemley

Camacho

et al. 2016

Animal

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“…Moreover, neonatal nutrition also influences gastrointestinal tract status, causing several disturbances in its structure, metabolism, and function (8). In this way, it has been shown that undernutrition affects villus height and crypt depth (9) as well as gastric emptying speed (10,11). Increased intestinal absorption of fatty acids and cholesterol has also been described in undernourished individuals refed with a high-fat diet (HFD) (12).…”

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confidence: 99%

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

et al. 2014

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Catch-up growth has been associated with the appearance of metabolic dysfunctions such as obesity and type 2 diabetes in adulthood. Because the entero-insular axis is critical to glucose homeostasis control, we explored the relevance of the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) in the development of these pathologies. Offspring of rat dams fed ad libitum (control [C]) or 65% food-restricted during pregnancy and suckling time (undernourished [U]) were weaned onto a high-fat (HF) diet (CHF and UHF, respectively) to drive catch-up growth. Both male and female UHF rats showed an obese phenotype characterized by hyperphagy, visceral fat accumulation, and adipocyte hypertrophy. High-fat diet induced deterioration of glucose tolerance in a sex-dependent manner. Female UHF rats experienced much more severe glucose intolerance than males, which was not compensated by insulin hypersecretion, suggesting insulin resistance, as shown by homeostatic model assessment of insulin resistance values. Moreover, female, but not male, UHF rats displayed enhanced GIP but not GLP-1 secretion during oral glucose tolerance test. Administration of the GIP receptor antagonist (Pro3)GIP to UHF female rats over 21 days markedly reduced visceral fat mass and adipocyte hypertrophy without variations in food intake or body weight. These changes were accompanied by improvement of glucose tolerance and insulin sensitivity. In conclusion, the exacerbated production and secretion of GIP after the catch-up growth seems to represent the stimulus for insulin hypersecretion and insulin resistance, ultimately resulting in derangement of glucose homeostasis. Overall, these data evidence the role of GIP as a critical link between catch-up growth and the development of metabolic disturbances. (Endocrinology 155: 3769 -3780, 2014)

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“…22 Our current observations are consistent with our previous findings, and the outcome of this study further provided evidence supporting a notion that disturbance of the entero-insular axis as a consequence of declined GLP-1 secretion and b-cell dysfunction may be responsible for the increased risk of metabolic disorders during CUG after food restriction in rodents. 21 Since GLP-1 has both b-cell trophic effects and extrapancreatic effects, the improved metabolic conditions in the CUG rat might also be contributed by the incretin-mediated improvement of lipid metabolism. 27 Notably, the CUG rats, whether they received liraglutide daily injections or not, showed significantly increased b-cell mass.…”

Section: Discussionmentioning

confidence: 99%

Liraglutide prevents fast weight gain and β-cell dysfunction in male catch-up growth rats

Zheng

Chen

Zhu

et al. 2015

Exp Biol Med (Maywood)

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We reported recently that after a nutritional growth retardation, rats showed significant weight gain, central fat accumulation, dyslipidemia, and b-cell dysfunction during a catch-up growth (CUG) phase. Here, we investigated whether glucagon-like peptide-1 (GLP-1) ameliorated the rapid weight gain, central fat deposition, and b-cell dysfunction during the CUG in rats. Sixty-four male Sprague Dawley rats were stratified into four groups including normal control group, CUG group, catch-up growth with liraglutide treatment group, and catch-up growth with liraglutide and exendin 9-39 treatment group. Energy intake, body weight, and body length were monitored. Fat mass percentage was analyzed by dual energy X-ray absorptiometry scan. Plasma triglyceride and non-esterified fatty acid were measured. The b-cell mass was analyzed by morphometric analysis and signaling molecules were examined by Western blot and real-time PCR. Insulin secretion capability was evaluated by hyperglycemic clamp test. Liraglutide prevented weight gain and improved lipid and glucose metabolism in rats under CUG conditions, which were associated with reduced fasting insulin levels and improved glucose-stimulated insulin secretion. Improved b-cell function is found to be associated with increased b-cell replication as determined by b-cell density and insulin-Ki67 dual staining. Furthermore, liraglutide increased islet pancreatic duodenal homeobox-1 (Pdx-1) and B-cell lymphoma-2 transcript and protein expression, and reduced Procaspase-3 transcript and Caspase-3 p11 subunit protein expression, suggesting that expression of Pdx-1 and reduction of apoptosis may be the mechanisms involved. The therapeutic effects were attenuated in rats co-administered with exendin 9-39, suggesting a GLP-1 receptor-dependent mechanism. These studies revealed that incretin therapy effectively prevented fast weight gain and b-cell dysfunction in rats under conditions of nutrition restriction followed by nutrition excess, which is in part due to enhanced functional b-cell mass and insulin secretory capacity.

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Effect of catch-up growth after food restriction on the entero-insular axis in rats

Cited by 15 publications

References 39 publications

Influence of nutrient restriction and melatonin supplementation of pregnant ewes on maternal and fetal pancreatic digestive enzymes and insulin-containing clusters

Influence of nutrient restriction and melatonin supplementation of pregnant ewes on maternal and fetal pancreatic digestive enzymes and insulin-containing clusters

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

Liraglutide prevents fast weight gain and β-cell dysfunction in male catch-up growth rats

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