Influence of low dietary lipid content on anorexia and [¹⁴C]glucose uptake in the intestine of zinc-deficient mice

Abstract

Zinc deficiency was induced in adult male mice by feeding them for 8 weeks on a purified semi-synthetic Zn-deficient diet (ZD) containing 90 g lipid/kg (60 g maize oil plus 30 g cod-liver oil). One group was then fed on a low-lipid Zn-deficient diet (ZDLR) containing 30 g cod-liver oil/kg as the sole lipid source for a further 8 weeks. At the end of the experiment the stomach clearance rate, daily food intake, body-weight gain and [14C]glucose uptake in the intestine were significantly higher in group ZDLR than in mice that continued eating the Zn-deficient lipid-adequate diet ZD, and were comparable to results for a group given a Zn-supplemented diet. These results suggest that the pathogenesis of anorexia, nutrient malabsorption and growth retardation are secondary to lipid malabsorption resulting from Zn deficiency

Lipid–zinc interaction: its effect on the testes of mice

“…Their Zn concentration in serum being identical, the excess lipid in diet group HFZD appears to have been responsible for the induction of Zn-deficiency-related symptoms. This is in accordance with our earlier report (Taneja & Arya, 1992). We reported that the symptoms appeared in mice when fed on a Zn-deficient diet containing cod-liver oil (30 g/kg) and maize oil (60 g/kg) as the lipid source and they disappeared, despite Zn deficiency, when the maize oil was withdrawn from the Zn-deficient diet.…”

“…We reported that the symptoms appeared in mice when fed on a Zn-deficient diet containing cod-liver oil (30 g/kg) and maize oil (60 g/kg) as the lipid source and they disappeared, despite Zn deficiency, when the maize oil was withdrawn from the Zn-deficient diet. The similarity of the results between the present study and the one reported previously (Taneja & Arya, 1992) clarifies that the quantity rather than quality of the fat induces the symptoms in Zndeficient mice. Associated with the reduction of body weight, significantly lower testes weights in the animals of group HFZD are in conformity with the observations of previous investigators who fed fat at 50 g/kg or above in the basal diet (Millar et al 1958;Bieri & Prival, 1966;Sandstead et al 1967;Abbasi et al 1976;Lei et al 1976;Underwood, 1977;Taneja & Nirmal, 1980;McClain et al 1984;Reeves, 1990).…”

“…Lipid deposition in the intestinal mucosal epithelial cells causes an inhibition of stomach emptying and gastric secretion through a feedback mechanism in rats (Konturek & Grossman, 1965;Long & Brooks, 1965). A similar mechanism appears to operate in mice as well which we determined by estimating the feed intake and stomach clearance in mice fed on a high-fat Zn-deficient diet (Taneja & Arya, 1992). It also exacerbated the malabsorption of nutrients by interfering with the intestinal uptake mechanism which we concluded by estimating [14C]glucose uptake (Taneja & Arya, 1992).…”

“…The low feed intake, loss of body weight and impairment of testicular function appeared only in response to Zn-deficiency coupled with a high fat concentration in the diet and not in response to a low fat concentration in the diet. In the absence of Zn in the diet, lipid has been observed to accumulate in the mucosal epithelial cells of the intestine of rats (Koo & Turk, 1977), mice (Taneja & Arya, 1992) and carp (Cyprinus carpio; Taneja et al 1990). Based on electron microscopic studies, Koo & Turk (1977) reported that the nascent chylomicrons in the Zn-deficient rats lost their stability and coalesced to form bigger droplets that were unable to pass to the lacteals.…”

“…Underwood (1977) suggested that the hormonal changes might be secondary to inanition and growth retardation effects caused by Zn deficiency. Taneja & Arya (1992) observed that the low feed intake and growth retardation effects caused by Z n deficiency were ameliorated by restricting the fat content to 30 g/kg in a Zn-deficient basal diet. This suggests that a high lipid content in a Zn-deficient diet is responsible for the induction of these symptoms and possibly may influence the testicular function so widely reported in Zn-deficient mammals.…”