Interesterification of olive oil with a fully hydrogenated fat in a batch reactor using step changes in temperature.

Interesterification of a 60:40 (wt/wt) mixture of olive oil and fully hydrogenated canola oil was carried out in a batch reactor using a commercial immobilized lipase from Thermomyces lanuginose as a biocatalyst. The effects of a stepwise change of temperature on the degree of conversion, the solid fat content (SFC) of the products, and the residual activity of the enzyme were investigated. As a reference condition, an interesterification trial was conducted at a constant temperature of 70 degrees C for 48 h. For trials in which a temperature of 70 degrees C was used for the first 4 h of reaction and a temperature of 60 degrees C was employed for the following 44 h, there were no significant differences (p < 0.05) in the overall degree of conversion relative to the reference condition. Oils interesterified for only 1 or 2 h at 70 degrees C had melting points higher than 60 degrees C, whereas an oil produced by interesterification at 70 degrees C for only 4 h had a melting point of 58 degrees C. There was little difference (p < 0.05) between the SFC profiles of the interesterification products prepared by two different temperature protocols (70 degrees C for 24 h; 70 degrees C for 4 h followed by 60 degrees C for 20 h). Use of the protocol involving a step decrease in temperature significantly decreased catalyst deactivation effects, thereby increasing the residual activity of the immobilized lipase.

Leptin gene expression and serum leptin levels in zinc deficiency: implications for appetite regulation in rats.

Zinc deficiency in animals causes impaired growth and anorexia, and the mechanisms for these symptoms of zinc deficiency are not yet clear. We investigated whether circulating leptin levels and gene expression would be dysregulated under zinc deficiency and what would be the implications for appetite in rats. In study 1, 24 Sprague-Dawley rats were provided consecutively with three different dietary zinc intake levels: Zn-adequate (30 mg/kg of diet), Zn-depleted (1 mg/kg of diet), and Zn-replete (50 mg/kg of diet), for 1, 2, and 2 weeks, respectively. At the end of each dietary period, one-third of the rats were killed. In study 2, rats were assigned to one of the four Zn diet groups: Zn-adequate (30 mg/kg of diet), pair-fed (30 mg/kg of diet), Zn-deficient (1 mg/kg of diet), or Zn-sufficient (50 mg/kg of diet), and were fed for 4 weeks. Tissue Zn and serum leptin were measured, and leptin gene expression in adipose tissues (inguinal and abdominal) was determined by reverse transcription-polymerase chain reaction and northern blotting. Blood subfractions as plasma, red blood cells, and mononuclear cells and liver Zn level were decreased during the Zn-depletion period (P <.05). Serum leptin showed a tendency to increase during the Zn-depletion period and decreased back to the level of the Zn-repletion period. Leptin mRNA levels in inguinal adipocytes also increased during the Zn-depletion (P <.05) and Zn-deficient periods, which is consistent with the change in serum leptin. However, the decrease in leptin mRNA in abdominal adipocytes was not consistent with the increase in inguinal leptin levels and the change in serum leptin. Increased leptin levels in linguinal adipocytes is consistent with the expected physiological change of a decrease in appetite under Zn deficiency. However, before coming to any firm conclusion, further studies on adipose tissue-specific leptin expression, including the appetite-related neuropeptides, are necessary for clarifying the cause of lower appetite in zinc deficiency.