Food and Behaviour Research

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The effect of peripheral administration of zinc on food intake in rats fed Zn-adequate or Zn-deficient diets.

Jing MY, Sun JY, Wang JF. (2008) Biol Trace Elem Res. 124(2): 144-56. Epub 2008 Apr 19 

Web URL: View this and related abstracts via PubMed here

Abstract:

Zinc deficiency induces a striking reduction of food intake in animals. To elucidate the mechanisms for this effect, two studies were connectedly conducted to determine the effects of peripheral administration of zinc on food intake in rats fed the zinc-adequate or zinc-deficient diets for a 3-week period.

In study 1, two groups of male Sprague-Dawley rats were provided diets made either adequate (ZA; 38.89 mg/kg) or deficient (ZD; 3.30 mg/kg) in zinc. In study 2, after feeding for 3 weeks, both ZA and ZD groups received intraperitoneal (IP) injection of zinc solution with three levels (0.5, 1.0, and 2.0 microg zinc/g body weight, respectively) and cumulative food intake at 0.5, 1, 2, 4, and 24 h, and plasma hormones concentrations were measured.

The results in study 1 showed rats fed the ZD diets revealed symptoms of zinc deficiency, such as sparse and coarse hair, poor appetite, susceptibility to surroundings, lethargy, and small movements. Zinc concentrations in serum, femur, and skeletal muscle of rats fed the ZD diets declined by 26.58% (P < 0.01), 27.32% (P < 0.01), and 24.22% (P < 0.05), respectively, as compared with ZA control group. These findings demonstrated that rat models with zinc deficiency and zinc adequacy had been fully established.

The results in study 2 showed that IP administration of zinc in both ZA and ZD rats did not influence food intake at each time points (P > 0.05), although zinc deficiency suppressed food intake. Plasma neuropeptide Y (NPY) was higher, but insulin and glucagon were lower in response to zinc deficiency or zinc administration by contrast with their respective controls (P < 0.05). Leptin, T3, and T4 concentrations were uniformly decreased (P < 0.05) in rats fed the ZD diets in contrast to ZA diets; however, no differences (P > 0.05) were observed during zinc injection. Calcitonin gene-related peptide was unaffected (P > 0.05) by either zinc deficiency or zinc administration.

The present studies suggested that zinc administration did not affect short-term food intake in rats even in the zinc-deficient ones; the reduced food intake induced by zinc deficiency was probably associated with the depression in thyroid hormones. The results also indicated that NPY and insulin varied conversely during the control of food intake.

FAB RESEARCH COMMENT:

This animal study confirms what many previous studies have shown - which is that zinc deficiency leads to a dramatic reduction in appetite and food intake, effectively causing both weight loss and other physical and behavioural features of anorexia.

It also showed that repletion of zinc (by infusion) did not restore normal appetite and food intake within a 24-hour period.

Short-term zinc treatment also failed to normalise the decreased levels of both leptin and thyroid hormones that were caused by the zinc deficient diet - leading researchers to conclude that these hormonal changes may help to explain the appetite-suppressing effects of zinc deficiency.

Human studies have also linked zinc deficiency with anorexia - and furthermore, there is preliminary evidence from clinical trials that zinc supplementation may help recovery. See: