Eggs as an affordable source of nutrients for adults and children living in food-insecure environments.

Food insecurity affects an estimated 12% of households in the United States. Adults and children who experience food insecurity are increased risk for development of metabolic diseases such as type 2 diabetes, obesity, and cardiovascular disease. The negative health outcomes associated with food insecurity are multifactorial; however, many of them may be caused by limited nutritional intake and poor diet quality. Dietary intake of eggs may be an applicable solution for food-insecure families who are challenged by limited nutritional intake. Eggs contain a variety of nutrients that support metabolic health. For instance, eggs are a complete source of high-quality protein and contain 16 vitamins and minerals. Furthermore, eggs are cost efficient. When comparing the relationship between foods on the basis of calories and unit cost, the energy cost of eggs is significantly less when compared with that of other animal-protein foods such as meat, poultry, and fish. However, dietary intake of eggs is controversial in regard to cardiovascular health. Thus, the aim of this review is to summarize the role of eggs in the diet and the impact eggs have on health for adults and children living in a food-insecure environment.

Diet-induced obesity alters anabolic signalling in mice at the onset of skeletal muscle regeneration.

AIM: Obesity is classified as a metabolic disorder that is associated with delayed muscle regeneration following damage. For optimal skeletal muscle regeneration, inflammation along with extracellular matrix remodelling and muscle growth must be tightly regulated. Moreover, the regenerative process is dependent on the activation of myogenic regulatory factors (MRFs) for myoblast proliferation and differentiation. The purpose of this study was to determine how obesity alters inflammatory and protein synthetic signalling and MRF expression at the onset of muscle regeneration in mice. METHODS: Forty-eight male C57BL/6J mice (3 weeks old) were randomly assigned to either a high-fat diet (HFD, 60% fat) or a lean diet (10% fat) for 12 weeks. At 15 weeks, bupivacaine was injected into the tibialis anterior (TA) of the injured group (n = 5-8/group) and PBS was injected into the control (n = 5-6). The TA was excised 3 or 28 days after injection. RESULTS: We demonstrated impaired muscle regeneration in obese mice. The obese mice had reduced IL-6, MyoD and IGF-1 mRNA abundance compared to the lean mice (P < 0.05). Three days following muscle damage, TNF-α mRNA and protein levels of P-STAT3 and P-Akt were 14-fold, fourfold and fivefold greater in the lean mice respectively. However, there were no differences observed in the obese injured group compared to the uninjured group. Moreover, p70S6K1 was threefold greater in lean injured mice compared to uninjured but was reduced by 28% in the obese injured mice. CONCLUSION: Obese mice have impaired inflammatory and protein synthetic signalling that may negatively influence muscle regeneration.