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Maternal protein restriction during gestation impairs female offspring pancreas development in the rat
Lizbeth Calzada1, Angélica Morales1, Tonantzin C Sosa-Larios1
1Department of Reproductive Biology, National Institute of Medical Science and Nutrition "Salvador Zubirán", Vasco de Quiroga 15 Col. Belisario Domínguez Sección XVI, Tlalpan, CP. 14080 Mexico City, Mexico.
Insights
Maternal low-protein diets alter offspring islet cell development, reducing beta cells and impacting pancreatic function later in life. This study reveals critical early-life programming effects on metabolic health.
Area of Science:
- Endocrinology
- Developmental Biology
- Metabolic Research
Background:
- Maternal low-protein (LP) diets during gestation are linked to offspring metabolic dysfunction.
- Prenatal nutrition influences fetal pancreatic islet development and function.
Purpose of the Study:
- To investigate how maternal protein restriction impacts pancreatic islet morphology and cellular composition in female offspring.
- To analyze changes in beta (β) and alpha (α) cell populations throughout postnatal development.
Main Methods:
- Offspring from control (20% casein) and LP (10% casein) maternal diets were studied at specific postnatal days (PNDs 7-110).
- Pancreatic tissues were analyzed using immunohistochemistry to quantify β and α cells.
- Islet size, cellular area, and β/α cell ratios were measured.
Main Results:
- Islet cytoarchitecture and total area remained similar between groups.
- LP offspring showed a lower proportion of β cells at early ages (PNDs 7-21).
- The β/α cell ratio was altered, being lower in LP offspring at PNDs 7 and 21, and higher at PND 36.
Conclusions:
- Maternal protein restriction alters offspring islet cell ontogeny, affecting β and α cell proportions.
- Reduced β cell numbers postnatally may have long-term implications for pancreatic function.
- Early-life nutritional programming by maternal diet significantly impacts offspring metabolic health trajectory.
Abstract:
A maternal low-protein (LP) diet programs fetal pancreatic islet β-cell development and function and predisposes offspring to metabolic dysfunction later in life. We hypothesized that maternal protein restriction during pregnancy differentially alters β- and α-cell populations in offspring by modifying islet ontogeny and function throughout life. We aimed to investigate the effect of an LP maternal diet on pancreatic islet morphology and cellular composition in female offspring on postnatal days (PNDs) 7, 14, 21, 36, and 110. Mothers were divided into 2 groups: during pregnancy, the control group (C) was fed a diet containing 20% casein, and the LP group was fed an isocaloric diet with 10% casein. Offspring pancreases were obtained at each PND and then processed. β and α cells were detected by immunohistochemistry, and cellular area and islet size were quantified. Islet cytoarchitecture and total area were similar in C and LP offspring at all ages studied. At the early ages (PNDs 7-21), the proportion of β cells was lower in LP than C offspring. The proportion of α cells was lower in LP than C offspring on PND 14 and higher on PND 21. The β/α-cell ratio was lower in LP compared with C offspring on PNDs 7 and 21 and higher on PND 36 (being similar on PNDs 14 and 110). We concluded that maternal protein restriction during pregnancy modifies offspring islet cell ontogeny by altering the proportions of islet sizes and by reducing the number of β cells postnatally, which may impact pancreatic function in adult life.
