Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood.

Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whether maternal consumption of a HFD during critical periods of development can lead to metabolic changes in the offspring metabolism. This study evaluated the potential effects of metabolic programming on the impairment of insulin signalling in recently weaned offspring from obese dams. Additionally, we investigated if early exposure to an obesogenic environment could exacerbate the impairment of glucose metabolism in adult life in response to a HFD. Swiss female mice were fed with Standard Chow (SC) or a HFD during gestation and lactation and tissues from male offspring were analysed at d28 and d82. Offspring from obese dams had greater weight gain and higher adiposity and food intake than offspring from control dams. Furthermore, they showed impairment in insulin signalling in central and peripheral tissues, which was associated with the activation of inflammatory pathways. Adipose tissue was ultimately the most affected in adult offspring after HFD rechallenge; this may have contributed to the metabolic deregulation observed. Overall, our results suggest that diet-induced maternal obesity leads to increased susceptibility to obesity and impairment of insulin signalling in offspring in early and late life that cannot be reversed by SC consumption, but can be aggravated by HFD re-exposure.

Local and serum levels of adipokines in patients with obesity after periodontal therapy: one-year follow-up.

AIM: This study evaluated the effects of scaling and root planing (SRP) on gingival crevicular fluid (GCF) and serum levels of adipokines in patients with chronic periodontitis (CP) with or without obesity. METHODS: Twenty patients with obesity and 20 patients without obesity, all with CP, received SRP. Serum and GCF levels of resistin, adiponectin, leptin, tumour necrosis factor [TNF]-α and interleukin [IL]-6 were evaluated by enzyme-linked immunosorbent assay at baseline, 3, 6 and 12 months post-therapy. RESULTS: SRP reduced the amounts of TNF-α in deep sites and increased the concentration of adiponectin in shallow sites of non-obese patients (p < 0.05). SRP increased the concentrations of TNF-α and leptin in patients with obesity (p < 0.05). GCF levels of TNF-α were higher in patients with obesity than in patients without obesity at all time-points (p < 0.05). There were no changes in serum levels of any adipokines for any group after therapy (p > 0.05). Patients with obesity exhibited higher serum levels of leptin at all time-points and IL-6 at 3 months post-therapy (p < 0.05). CONCLUSIONS: Obesity may modulate systemic and periodontal levels of adipokines in favour of pro-inflammation, independently of periodontal therapy. SRP did not affect the circulating levels of adipokines in patients with or without obesity.