Breastfeeding duration is associated with higher adiposity at 6-8 months of age.

Breastfeeding (BF) has been identified as a protective factor against childhood obesity. However, evidence of the association between BF duration and adiposity remains inconclusive. Few studies have been conducted among Southeast Asian infants that have measured body composition during infancy using the gold standard stable isotope method. This study aimed to evaluate the association between BF duration and body composition during infancy. Healthy full-term Thai infants aged 6-8 months (n = 60) receiving exclusive or predominant BF for at least 3 months were recruited. Skinfold thickness (SFT) was measured by well-trained investigators. Body composition was assessed by the deuterium dilution technique. Infants with longer BF duration (>6 months; mean 7.5 ± 0.5 months, n = 29) had a higher subscapular SFT z-score than those with shorter BF duration (≤6 months; mean 5.3± 0.9 months, n = 31) by 0.48 (95% confidence interval [CI]: 0.01-0.94). After adjustment for age and sex, BF duration and age at introduction of complementary feeding (CF) were positively associated with fat mass and fat mass index at 6-8 months. One month increase in BF duration and CF age was associated with a 0.37 (95% CI: 0.05, 0.69) kg/m2 and 0.76 (95% CI: 0.18, 1.34) kg/m2 increase in the fat mass index, respectively. After adjusting for infant body mass index (BMI) during the earlier infancy period, the strength of the association was attenuated. This finding may reflect reverse causality where infants with lower BMI received formula or CF earlier. A longitudinal study with follow-up into childhood is warranted to confirm the effects of BF on adiposity in infancy and childhood.

Morphological alteration of the pancreatic islet in ovariectomized rats fed a high-fat high-fructose diet.

Diabetes and its complications are major causes of mortality worldwide. Type 2 diabetes coexists with insulin resistance and ß-cell dysfunction, which are aggravated by overconsumption and estrogen-deprived conditions. However, the morphology of pancreatic islets in a combined condition of excessive caloric intake and estrogen deficiency has never been described. Herein, we examined morphological changes in the pancreatic islets of ovariectomized (OVX) rats fed a high-fat high-fructose diet (HFFD) for 12 weeks. The histological changes in the size and number of pancreatic islets were assessed by hematoxylin-eosin and immunohistochemical staining. Enlarged pancreatic islets with fat deposition in OVX rats were accompanied by whole-body insulin resistance and hyperglycemia. The addition of a HFFD to OVX rats (OVX + HFFD) further aggravated insulin resistance, with a substantial increase in the density of enlarged pancreatic islets and fat accumulation. The augmented number of enlarged islets was correlated with elevated plasma glucose and insulin levels. Intriguingly, unlike the HFFD and OVX alone, the OVX + HFFD markedly expanded the area of insulin-producing ß-cells and glucagon-producing α-cells. Importantly, enlarged islets, pancreatic fat deposits, and diabetic states developing in OVX + HFFD conditions were resolved by estrogen replacement. Collectively, the morphological characteristics of pancreatic islets were influenced in an insulin-resistant state caused by estrogen deficiency and HFFD consumption and were distinct from each factor alone. A combination of estrogen deficiency with HFFD consumption worsened the integrity of pancreatic islets, ultimately resulting in disease progression. These findings expand our understanding of the causal relationship between pancreatic morphology and diabetes development and suggest therapeutic strategies.