AI Article Synopsis
- Early weaning (EW) in lactating rats leads to changes in gut peptides, specifically glucagon-like peptide 1 (GLP-1), which may contribute to obesity and related health issues later in life.
- A study found that EW rats had higher levels of GLP-1 in their plasma and tissues, but lower levels in their gut, and calcium supplementation was shown to restore normal GLP-1 responses and receptor levels.
- The findings suggest that EW has both immediate and lasting impacts on GLP-1 regulation and appetite control, with calcium supplementation potentially mitigating these negative effects.
Article Abstract
Scope: Gut peptides regulate appetite and adipogenesis. Early weaning (EW) leads to later development of obesity that can be prevented by calcium supplementation. We evaluated gut peptides that may have a role in the establishment of this dysfunction.
Methods And Results: At birth, lactating Wistar rats were separated in: EW, lactating rats involved with a bandage interrupting the lactation during the last 4 days of standard lactation, and C (control) dams whose pups had free access to milk during throughout lactation. At 120 days old, half of EW group received calcium supplementation (EWCa); EW and C received standard diet. At 21 days old, EW presented higher glucagon-like peptide 1 (GLP-1) in plasma and glucagon-like peptide 1 receptor (GLP1-R) in adipose tissue and hypothalamus, but lower GLP-1 and GLP1-R in the gut. At 180 days old, GLP-1 response to food intake was blunted in EW and restored by calcium. GLP-1 in the gut was lower in EW and its receptor was lower in adipose tissue, and GLP1-R was higher in the gut of calcium EW group.
Conclusion: Thus, EW had short- and long-term effects upon GLP-1 profile, which may have contributed to obesity development, hyperphagia, and insulin resistance due to its adipogenic and appetite control roles. Calcium supplementation was able to prevent most of the changes in GLP-1 caused by EW.
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| http://dx.doi.org/10.1002/mnfr.201400666 | DOI Listing |
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