leptin and Deficiency-Diseases

Zinc is required by humans and animals for many physiological functions, such as growth, immune function, and reproduction. Zinc deficiency induces a number of physiological problems, including anorexia, growth retardation, dermatitis, taste disorder, and hypogonadism. Although it is clear that zinc deficiency produces specific and profound anorexia in experimental animals, the connection between zinc deficiency and anorexia is less certain. We were the first to show that orally, but not intraperitoneally, administered zinc rapidly stimulates food intake through orexigenic peptides coupled to the afferent vagus nerve using rats during early-stage zinc deficiency without decreased zinc concentrations in plasma and tissues. We confirmed that a zinc-sufficient diet containing zinc chloride acutely stimulated food intake after short-term zinc deprivation. We also found that orally administered zinc sulfate increased the expression of NPY and orexin mRNA after administration. Using vagotomized rats, we tested whether the increase in food intake after oral administration of zinc was mediated by the vagus nerve. In sham-operated rats, the oral administration of zinc stimulated food intake, whereas zinc and saline administrations did not exhibit differing effects in vagotomized rats. We conclude that zinc stimulates food intake in short-term zinc-deficient rats through the afferent vagus nerve with subsequent effects on hypothalamic peptides associated with food intake regulation. In this review, we describe recent research investigating the roles of zinc as an appetite stimulator in food intake regulation, along with research about hypothalamus, ghrelin, leptin and zinc receptor, and clinical application about anorexia nervosa, cachexia and sarcopenia. The article also presents some promising patents on zinc.

Topics: Animals; Anorexia Nervosa; Appetite; Cachexia; Deficiency Diseases; Energy Intake; Ghrelin; Humans; Hypothalamus; Leptin; Patents as Topic; Sarcopenia; Trace Elements; Zinc

Some epidemiologic studies have suggested inverse relations between intake of dairy products and components of the metabolic syndrome.. The objective was to investigate the effects of an increased intake of dairy products in persons with a habitually low intake on body composition and factors related to the metabolic syndrome.. Middle-aged overweight subjects (n = 121) with traits of the metabolic syndrome were recruited in Finland, Norway, and Sweden and randomly assigned into milk or control groups. The milk group was instructed to consume 3-5 portions of dairy products daily. The control group maintained their habitual diet. Clinical investigations were conducted on admission and after 6 mo.. There were no significant differences between changes in body weight or body composition, blood pressure, markers of inflammation, endothelial function, adiponectin, or oxidative stress in the milk and the control groups. There was a modest unfavorable increase in serum cholesterol concentrations in the milk group (P = 0.043). Among participants with a low calcium intake at baseline (<700 mg/d), there was a significant treatment effect for waist circumference (P = 0.003) and sagittal abdominal diameter (P = 0.034). When the sexes were analyzed separately, leptin increased (P = 0.045) and vascular cell adhesion molecule-1 decreased (P = 0.001) in women in the milk group.. This study gives no clear support to the hypothesis that a moderately increased intake of dairy products beneficially affects aspects of the metabolic syndrome. The apparently positive effects on waist circumference and sagittal abdominal diameter in subjects with a low calcium intake suggest a possible threshold in relation to effects on body composition.

Topics: Adult; Aged; Calcium, Dietary; Cholesterol; Dairy Products; Deficiency Diseases; Diet; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Female; Finland; Humans; Leptin; Male; Metabolic Syndrome; Middle Aged; Norway; Overweight; Sex Factors; Sweden; Vascular Cell Adhesion Molecule-1; Waist Circumference

Leptin is an adipose-derived hormone that primarily regulates energy balance in response to nutrition. Human placental cells produce leptin, whereas murine placental cells produce soluble leptin receptors (Ob-R). However, the roles of these proteins during pregnancy have not been elucidated completely. As an essential metal, zinc (Zn) is central to insulin biosynthesis and energy metabolism. In the present study, the effects of Zn deficiency and supplementation on maternal plasma leptin and soluble Ob-R regulation in pregnant mice placentas were examined using enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blotting. Nutritional Zn deficiency significantly reduced plasma insulin concentrations and fetal and placental weights in pregnant mice. Plasma leptin concentrations in pregnant mice also increased 20- to 40-fold compared with those in non-pregnant mice. Although dietary Zn deficiency and supplementation did not affect plasma leptin concentrations in non-pregnant mice, Zn-deficient pregnant mice had significantly reduced plasma leptin concentrations and adipose leptin mRNA expression. In contrast, Zn-supplemented pregnant mice had increased plasma leptin concentrations without increased adipose leptin mRNA expression. Placental soluble Ob-R mRNA expression also decreased in Zn-deficient mice and tended to increase in Zn-supplemented mice. These results indicate that Zn influences plasma leptin concentrations by modulating mRNA expression of soluble Ob-R in the placenta, and leptin in visceral fat during pregnancy. These data suggest that both adipose and placenta-derived leptin system are involved in the regulation of energy metabolism during fetal growth.

Topics: Adipose Tissue; Animals; Blood Glucose; Deficiency Diseases; Dietary Supplements; Female; Fetal Development; Gene Expression; Glucose Transporter Type 1; Insulin; Leptin; Mice; Organ Size; Placenta; Pregnancy; Receptors, Leptin; Zinc

To investigate the change of leptin, adiponectin and visfatin levels in adult growth hormone deficiency (GHD) patients, and its relationship with other indicators.. 40 adult GHD patients (19 males) entered the observation group with 36 cases of healthy individuals (18 males) as the control group. Basic information (height, body mass, waistline, hipline etc.) was collected from both groups. Fasting venous blood samples were collected to measure the leptin, adiponectin and visfatin levels.. The GHD group had a higher waist to hip ratio, and higher levels of cholesterol, triglyceride (TG), low density lipoprotein cholesterol (LDL-C), leptin, adiponectin and visfatin, but lower levels of growth hormone (GH), insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3) and dehydroepiandrosterone sulfate (DHEA-S) when campared with that of the control group (P < 0.05). Logistic regression analysis demonstrated that adult GHD patients are associated with elevated levels of visfatin (OR = 1. 430, P < 0.05).. Our study implied that adult GHD patients are associated with elevated levels of visfatin.

Topics: Adiponectin; Adult; Case-Control Studies; Deficiency Diseases; Female; Growth Hormone; Humans; Leptin; Male; Middle Aged; Nicotinamide Phosphoribosyltransferase; Young Adult

Omega-3 polyunsaturated fatty acid deficiency, particularly during the prenatal period, can cause hypertension in later life. This study examined the effect of different sources of alpha-linolenic acid (canola oil or flaxseed oil) in the prevention of hypertension and other metabolic symptoms induced by an omega-3 fatty acid-deficient diet. Dams were provided one of three experimental diets from 1 week before mating. Diets were either deficient (10% safflower oil-DEF) or sufficient (7% safflower oil+3% flaxseed oil-SUF-F; or 10% canola oil-SUF-C) in omega-3 fatty acids. The male offspring were continued on the maternal diet from weaning for the duration of the study. Body weight, ingestive behaviors, blood pressure, body composition, metabolic rate, plasma leptin and brain fatty acids were all assessed. The DEF animals were hypertensive at 24 weeks of age compared with SUF-F or SUF-C animals; this was not evident at 12 weeks. These results suggest that different sources of ALA are effective in preventing hypertension related to omega-3 fatty acid deficiency. However, there were other marked differences between the DEF and, in particular, the SUF-C phenotype including lowered body weight, adiposity, leptin and food intake in SUF-C animals. SUF-F animals also had lower, but less marked reductions in adiposity and leptin compared with DEF animals. The differences observed between DEF, SUF-F and SUF-C phenotypes indicate that body fat and leptin may be involved in omega-3 fatty acid deficiency hypertension.

Topics: alpha-Linolenic Acid; Animal Feed; Animals; Blood Pressure; Body Composition; Body Weight; Brain; Calorimetry; Deficiency Diseases; Energy Metabolism; Fatty Acids, Monounsaturated; Female; Heart Rate; Hypertension; Leptin; Linseed Oil; Male; Pregnancy; Prenatal Exposure Delayed Effects; Rapeseed Oil; Rats; Rats, Sprague-Dawley; Safflower Oil

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.

Topics: Animals; Calcitonin Gene-Related Peptide; Deficiency Diseases; Dietary Supplements; Eating; Glucagon; Insulin; Leptin; Male; Neuropeptide Y; Rats; Rats, Sprague-Dawley; Thyroxine; Triiodothyronine; Zinc

For lactating dairy cows, we need management tools, that are "clean, green and ethical", cost-effective and easy to use. Specific tools are needed for artificial insemination (AI) after oestrus detection within a few months of calving, and for managing the complex nutritional requirements of cows between successive calvings. Assessment of energy deficit by measurement of body condition score (BCS) has been useful in the past but we now need more sophisticated ways to measure the relationship between adipose tissue and fertility. For this reason, we have focused our attention on the cells of the adipose tissue, the adipocytes, and the role of the hormone that they produce, leptin. This hormone affects pulsatile LH release and, in dairy cows, it seems to be linked to the first postpartum ovulation. Adipocytes are always sensing energy status and they control leptin secretion dynamically, so blood leptin concentrations can change acutely, even when there is no detectable change in BCS. Leptin secretion seems to be determined by the secretory activity of each adipocyte as well as the total mass of adipocytes in the body of the animal (as measured by BCS). The strong relationship between BCS, leptin concentration and reproductive function in dairy cows suggests that we should reconsider the interval of the recovery from prepartum and postpartum damages, the need for high milk yields at the last lactation causing the dry-off stress and the subsequent troubles. We should also re-assess the current drive to reduce calving interval because milk yields during the early stages of lactation are economically very important but high yields seem to cause several metabolic and reproductive disorders in modern dairy cows. In general, the thinking has been that calving interval must be short because short intervals are more profitable. However, if we remember that main product from dairy cows is milk and that a short calving interval is very difficult without reproductive problems, then a longer calving interval might be more sensible and also more profitable. We have example of an extended calving interval in Japan, Supercows which are very rare cows yielding remarkable high milk. Finally, we probably need to improve dairy cows genetically if we are to achieve the goal of "clean, green and ethical" dairy farming. This paper reviews data relevant to these strategies and we conclude that more basic and applied research will be required if we are to find ways to reach that g

Topics: Animal Husbandry; Animals; Body Composition; Cattle; Dairying; Deficiency Diseases; Female; Humans; Lactation; Leptin; Luteinizing Hormone; Maternal Nutritional Physiological Phenomena; Mice; Ovulation; Postpartum Period; Pregnancy; Reproduction; Ruminants; Time Factors

The present study was conducted to measure ob mRNA abundance in the zinc-deficient (ZD) rats and the secretion of leptin from adipose tissue obtained from ZD, zinc-adequate (ZA), and pair-fed (PF) rats. It was found that ob mRNA abundance was greatest (P < 0.05) in adipose tissue obtained from ZA and PF rats. Ob mRNA abundance was similar in PF and ZD rats. To study leptin secretion from adipose tissue in a cell culture model, a method was developed to use excised epididymal adipose tissue from ZD, ZA, and PF rats. Tissue was incubated in Opti-modified Eagle's medium (MEM) cell culture medium in which concentrations of zinc and insulin were manipulated. It was observed that leptin secretion was higher (P < 0.05) in adipose tissue obtained from ZA than ZD and PF rats. Secretion of leptin was higher in adipose tissue of PF than ZD rats (P < 0.05). Surprisingly, media zinc content in this ex vivo model tended to suppress secretion of leptin. This suppression seems to be zinc specific and might be caused by the sequestration of insulin in the culture medium. Our results indicate that the reduction in serum leptin observed in ZD rats is likely caused by not only a reduction in body fat, but also by a decrease in leptin synthesis and secretion per gram of adipose tissue. Taking these results into account along with a prior study (1), it is possible that even a marginal zinc deficiency could affect leptin secretion and serum leptin concentrations. Impaired leptin secretion caused by zinc deficiency might be one factor contributing to hypogonadism observed in zinc deficiency.

Topics: Adipocytes; Animals; Blotting, Northern; Deficiency Diseases; Gene Expression Regulation; Insulin; Leptin; Male; Pentetic Acid; Rats; Rats, Sprague-Dawley; RNA, Messenger; Zinc

Topics: Deficiency Diseases; Drug Resistance; Female; Growth Disorders; Humans; Hypothyroidism; Leptin; Obesity; Risk Assessment