Tissue-Specific Alterations in Lipoprotein Lipase Activity in Copper-Deficient Rats

Abstract

Copper deficiency results in alterations in lipid metabolism that include elevations in serum cholesterol and triglycerides and a decrease in whole-body respiratory quotient. Copper-deficient animals are also leaner even though electron micrographs of the myocardium present increased lipid droplet accumulation. To address whether a compromised copper status impacts triglyceride deposition in a tissue-specific manner, the activity of lipoprotein lipase was measured in adipose tissue and cardiac and skeletal muscle. Weanling rats fed a copper-restricted diet (<1 ppm) for 6 wk demonstrated a greater than twofold increase in cardiac lipoprotein lipase activity concomitant with a significant reduction in adipose tissue lipoprotein lipase activity. Skeletal muscle lipoprotein lipase activity was not altered by the copper-deficient state. The results of this study suggest that copper deficiency may induce a tissue-specific alteration in lipoprotein lipase activity in rats, which may contribute to the notable deposition of lipid substance in myocardium and the concomitant general body leanness.

Maternal blood cadmium, lead and arsenic levels, nutrient combinations, and offspring birthweight

“…While metabolic syndrome is not clinically discernible in young children [86], individual cardiometabolic risk markers that include central adiposity, elevated systolic blood pressure and elevated levels of fasting insulin and/or glucose, triglycerides, cholesterol, accelerated adiposity, [87–91, 76–78, 92–95] sometimes without overt obesity [96], predict metabolic syndrome, atherosclerosis, diabetes and hypertension in adulthood [97–104]. While not confirmed by others [47], increased adiposity and higher insulin have been associated with deficiency of Cu [36], Fe [37–40], Mn [41], Mg [42–44] and Zn [45, 46]. Thus, the low birthweight that is associated with early exposure to these toxic metals supports the developmental origins of these cardiometabolic diseases, and may portend, and/or contribute to the increase in incidence of these diseases.…”

“…For example, iron (Fe) deficiency in humans has been linked to elevated levels of Cd in both blood and urine, independent of smoking, poverty, age, race, obesity and parity [35]. Deficiencies in essential metals including Cu [36], Fe [37–40], manganese (Mn) [41] and magnesium (Mg) [42–44], and zinc (Zn) [45, 46] have been associated with increased risk of low birth weight and adiposity in some, but not all investigations [47, 48]. In animals, deficiencies in folate (a one-carbon cycle nutrient critical to the generation of S-adenosyl methionine, the universal methyl group donor) reduce As methylation and excretion [49].…”

The Role of Copper as a Modifier of Lipid Metabolism

“…Young, weanling rats fed on a copper deficient diet for six weeks are leaner than controls, though they have increased serum cholesterol and triglycerides. Metabolically, whole body respiratory quotient decreases, reflected in a reduction of cardiac and adipose lipoprotein lipase, but not the skeletal muscle lipoprotein lipase (55). The change in fuel use may be related to upregulation of fatty acid synthesis.…”

An Examination of the Association of Selected Toxic Metals with Total and Central Obesity Indices: NHANES 99-02

“…In mice, zinc deficiency induced by a mutation in the Znt7 zinc transporter caused a reduced body weight gain that was largely due to the decrease in body fat accumulation [3]. In contrast, deficiency of other essential metals, chromium [4,5], copper [6], iron [7,8], and magnesium [9], causes an increase in adiposity. The toxic metals, lead and cadmium are ubiquitous environmental toxins that are related to a broad range of physiologic, biochemical, and behavioral dysfunctions[10,11] and recent epidemiologic studies have reported that environmental exposure to lead or cadmium concentration has a graded association with several disease outcomes such as hypertension, peripheral artery diseases, kidney diseases, and cognitive impairment [12–17].…”