Neil F. Shay

Soy protein and isoflavones: their effects on blood lipids and bone density in postmenopausal women.

The effects of soy protein (40 g/d) containing moderate and higher concentrations of isoflavones on blood lipid profiles, mononuclear cell LDL receptor messenger RNA, and bone mineral density and content were investigated in 66 free-living, hypercholesterolemic, postmenopausal women during a 6-mo, parallel-group, double-blind trial with 3 interventions. After a control period of 14 d, during which subjects followed a National Cholesterol Education Program Step I low-fat, low-cholesterol diet, all subjects were randomly assigned to 1 of 3 dietary groups: Step I diet with 40 g protein/d obtained from casein and nonfat dry milk (CNFDM), Step I diet with 40 g protein/d from isolated soy protein containing 1.39 mg isoflavones/g protein (ISP56), or Step I diet with 40 g protein/d from isolated soy protein containing 2.25 mg isoflavones/g protein (ISP90). Total and regional bone mineral content and density were assessed. Non-HDL cholesterol for both ISP56 and ISP90 groups was reduced compared with the CNFDM group (P < 0.05). HDL cholesterol increased in both ISP56 and ISP90 groups (P < 0.05). Mononuclear cell LDL receptor mRNA was increased in subjects consuming ISP56 or ISP90 compared with those consuming CNFDM (P < 0.05). Significant increases occurred in both bone mineral content and density in the lumbar spine but not elsewhere for the ISP90 group compared with the control group (P < 0.05). Intake of soy protein at both isoflavone concentrations for 6 mo may decrease the risk factors associated with cardiovascular disease in postmenopausal women. However, only the higher isoflavone-containing product protected against spinal bone loss.

Zinc Deficiency Suppresses Plasma Leptin Concentrations in Rats

Leptin concentrations during zinc deficiency were measured. Leptin is produced by adipose tissue and has potent affects on body weight and food intake regulation. Zinc deficiency results in anorexia, but the cause for this anorexia is not well understood. Aberrant regulation during zinc deficiency of leptin expression or secretion could be a factor in this anorexia. Two groups of Sprague-Dawley male rats were provided AIN-93-based diets made either adequate or deficient in zinc (+Zn, −Zn; 30 or 1 mg Zn/kg diet) and a third group (PF) was provided the +Zn diet at the reduced levels consumed by −Zn rats. In Study 1, +Zn, −Zn, and PF rats (n = 12 ea.) were fed using a 4-hr meal-feeding protocol for 4, 9, and 28 days. Leptin concentrations in −Zn rats were lower than both +Zn and PF groups (P < 0.05) on Days 9 and 28. In Study 2, 24 rats were divided into −Zn (n = 6), +Zn (n = 6), and PF (n = 12) groups. On day 21, six PF rats were provided a meal (PF-fed: PF-F); the other six PF rats were not offered this final meal (PF-restricted: PF-R). Plasma leptin concentrations were again lowest in the −Zn group. Reduced leptin levels during zinc deficiency suggest that leptin is responding normally, signaling low body fat levels during zinc deficiency. It seems that leptin is not a dominant factor in the development of zinc deficiency-induced anorexia.

Food Intake Patterns Are Altered During Long-Term Zinc Deficiency in Rats

Rats experience anorexia and reduction or cessation in growth after being provided a zinc-deficient diet. While zinc deficient, intake levels may be reduced 50% or more compared to control rats. In the present report, diurnal food intake patterns of male Sprague-Dawley rats were measured during zinc deficiency. In Study 1, rats consuming a modified AIN-93 diet were tested during the dark phase using an automated food weighing system. In zinc-deficient animals (Zn-), the onset of the first meal of the dark phase was delayed compared to zinc-adequate rats (Zn+; 106+/-47 vs. 23+/-5 min; p<0.05) and the number of meals consumed during the dark phase was reduced in Zn- vs. Zn+ rats (3.9+/-0.5 vs 7.1+/-0.4; p<0.05). In Study 2, diurnal food intake patterns were tested using a three-choice macronutrient self-selection paradigm of carbohydrate-, protein-, and fat-containing diets made deficient or adequate in zinc (1 or 30 mg Zn/kg diet). Food intake was recorded in the early-, mid-, late-dark period (4 h each) and light period (12 h). Carbohydrate intake was 70% of total intake of both Zn+ and Zn- rats during the first 5 days, but decreased significantly to 50% in the Zn- group during the last 5 days. Fat intake increased significantly in the Zn- group during the last 5 days. This increase was the result of 4 of 15 Zn- rats increasing their intake of fat significantly. Results of this study indicate that zinc status alters dark phase and macronutrient selection patterns by delaying consumption of the initial meal of the dark phase, reducing the average meal number and by changing the dominant macronutrient preference of some Zn- rats.

Noradrenergic activity in the paraventricular nucleus and macronutrient choice during early dark onset by zinc deficient rats

Abstract Carbohydrate is a preferred macronutrient of rats during the early dark phase and associated with an increase in norepinephrine (NE) and neuropeptide Y (NPY) in the paraventricular nucleus (PVN). Macronutrient choice is altered during zinc deficiency (ZD). The relationship between NE activity in the PVN and macronutrient choice during early dark was evaluated in rats fed zinc adequate (ZA) or ZD diet for 14 days. Total caloric intake was similar for ZA and ZD groups (∼20 kJ) but ZA rats selected 63 ± 5% of calories as carbohydrate while ZD rats selected 53 ± 5% of their calories from protein (p < 0.01). Pair-fed (PF) rats selected 62 ± 5% of calories as carbohydrate. Noradrenergic activity was lower (p < 0.01) in ZD and PF compared to ZA. The association between increased NE in the PVN at dark onset and selection of carbohydrate is not supported by the present results.