Biomedical subjects

C M Kotz

Publications and source records attributed to C M Kotz.

28 records · Page 2Linked to original sources

PubMed1997

Lactation decreases mRNA levels of opioid peptides in the arcuate nucleus of the rat.

The state of lactation results in increased food intake to compensate for the increased energy expenditure to produce nutrients supplied to the offspring. In this study, Sprague-Dawley female rats lactating for 10-16 days, and rats 7 days post-lactation were implanted with osmotic minipumps infusing either naltrexone (NTX) (70 microg/h) or saline (0.9%) over a 48 h period. mRNA levels of pro-dynorphin (proDYN), pro-opiomelanocortin (POMC) and pro-enkephalin (proENK) were measured in the arcuate nucleus (ARC) and whole pituitary of both groups. In both saline- and NTX-treated lactating subjects, food intake was higher than in post-lactating subjects (P < 0.01). In post-lactating subjects, NTX decreased food intake by 27% during the infusion period (P < 0.05). There were no significant differences in body weight between the treatment groups; however, naltrexone decreased body weight gain in both lactating and post-lactating subjects. In both saline and NTX-treated lactating subjects, ARC mRNA levels of proDYN, POMC and proENK were significantly decreased compared with the saline or NTX-treated post-lactating subjects (P < 0.01). NTX did not significantly influence gene expression of opioid peptides in the ARC in either the lactating or the post-lactating subjects. Neither the lactation condition nor NTX administration significantly changed mRNA levels of proDYN, POMC or proENK in whole pituitary. Thus, as has been noted in energy-deprived rats, opioid peptide gene expression is decreased in the ARC of lactating rats, a period during which rats have increased energy requirements.

Animals↗

PubMed1997

Opioids in the nucleus of the solitary tract are involved in feeding in the rat.

We evaluated the effect of selective opioid peptides and naltrexone on feeding when injected into the nucleus of the solitary tract (NTS). Doses of 0, 1, 2, 4, and 8 nmol of [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAMGO, mu-agonist), dynorphin A-(1-17) (DynA-(1-17), kappa-agonist), and [D-Ser2]leucine enkephalin-thr, (delta-agonist) were injected into the NTS in satiated male rats, and food intake was measured at 1, 2, and 4 h. Only DAMGO significantly increased feeding above control levels at doses of 2, 4, and 8 nmol. Doses of 10 and 50 microg naltrexone in the NTS significantly decreased 18-h deprivation-induced feeding. These data suggest that NTS opioid receptors (primarily mu) may be involved in the regulation of feeding.

Analgesics↗

PubMed1997

Effect of naltrexone on feeding, neuropeptide Y and uncoupling protein gene expression during lactation.

Neuropeptide Y increases feeding and decreases measures of brown adipose tissue thermogenesis. In lactating rats, increased feeding, increased hypothalamic neuropeptide Y neuroactivity and decreased thermogenesis occur. Naltrexone is an opioid receptor antagonist which decreases neuropeptide Y-induced feeding and reverse neuropeptide Y-induced decreases in brown adipose tissue thermogenesis. We hypothesized that opioid receptors are involved in neuropeptide Y neuroactivity during lactation. To see if naltrexone would alter feeding neuropeptide Y gene expression in the arcuate nucleus, neuropeptide Y levels in the paraventricular nucleus, and uncoupling protein gene expression in brown adipose tissue of lactating rats, osmotic minipumps pre-filled with either 0.9% saline or naltrexone (70 micrograms/h) were implanted subcutaneously in 47 female Sprague-Dawley rats weighing 309 +/- 5 g. Half these rats were studied on days 10-16 of lactation, and the other half were studied 7 days after lactation. After 48 h, neuropeptide Y mRNA levels and uncoupling protein mRNA levels were determined using specific cDNA probes. Neuropeptide Y peptide levels in the paraventricular nucleus were measured by radioimmunoassay. Naltrexone decreased food intake by 26% in the postlactating rats, but had no effect on feeding in the lactating animals. Lactation resulted in significantly increased arcuate neuropeptide Y mRNA, decreased neuropeptide Y levels in the paraventricular nucleus and decreased brown adipose tissue uncoupling protein mRNA levels. Naltrexone did not influence any of these parameters. Thus, the alterations in neuropeptide Y neuroactivity and brown fat thermogenesis which occur in lactation is not altered by generalized opioid receptor blockade.

Animals↗

PubMed1996

Naltrexone induces arcuate nucleus neuropeptide Y gene expression in the rat.

Neuropeptide Y (NPY) has potent effects on several components of energy metabolism, including increased feeding and decreased brown fat thermogenesis. Negative energy balance, such as food deprivation, increases NPY mRNA in hypothalamic arcuate nucleus (ARC). Naltrexone (NLTX), an opioid receptor antagonist, decreases NPY-induced feeding. We hypothesized that NLTX would alter ARC NPY mRNA and change NPY effects on brown fat. Osmotic minipumps prefilled with either saline or NLTX (70 micrograms/h) were implanted subcutaneously in 32 male Sprague-Dawley rats. One-half of the rats were food deprived and one-half were allowed food ad libitum for 48 h. Food intake was measured at 24 and 48 h. At 48 h, ARC NPY mRNA and brown fat uncoupling protein (UCP) mRNA levels were determined using cDNA probes. Forty-eight-hour food intake was significantly decreased by 24% after NLTX infusion. Food deprivation and NLTX treatment significantly and independently increased ARC NPY mRNA and decreased UCP mRNA levels in brown fat, suggesting a complex interaction between hypothalamic NPY and endogenous opioids in the regulation of energy balance.

Adipose Tissue, Brown↗

PubMed1995

Effects of opioid antagonists naloxone and naltrexone on neuropeptide Y-induced feeding and brown fat thermogenesis in the rat. Neural site of action.

Neuropeptide Y administered intracerebroventricularly and into the paraventricular nucleus of the hypothalamus stimulates feeding and decreases brown adipose tissue thermogenesis. Although specific neuropeptide Y antagonists are not yet available, previous studies had shown that the opioid antagonist naloxone blocked neuropeptide Y-induced feeding when both drugs were injected intracerebroventricularly. We wanted to find out if naloxone injected into specific brain sites would block neuropeptide Y effects on feeding and brown fat thermogenesis. Rats were double injected in specific brain sites with neuropeptide Y and either naloxone or naltrexone (a congener of naloxone). Food intake and brown fat measures were assessed. Naloxone or naltrexone in the paraventricular nucleus weakly decreased paraventricular nucleus neuropeptide Y-induced feeding and did not affect neuropeptide Y-induced reductions in brown fat activity. Peripheral naloxone blocked intracerebroventricular neuropeptide Y-induced feeding and brown fat alterations. Fourth ventricular naloxone decreased paraventricular nucleus neuropeptide Y-induced feeding, and naltrexone given into the nucleus of the solitary tract blocked paraventricular nucleus neuropeptide Y-induced alterations in feeding and brown fat. These data indicate that neuropeptide Y in the paraventricular nucleus may act on feeding and brown fat thermogenesis through opioidergic pathways in the nucleus of the solitary tract.

Adipose Tissue, Brown↗

PubMed1994

Rat hypothalamic NPY mRNA and brown fat uncoupling protein mRNA after high-carbohydrate or high-fat diets.

We measured the influence of diet composition on hypothalamic neuropeptide Y (NPY) message and brown fat uncoupling protein (UCP) mRNA using different diets. Sprague-Dawley rats ate ad libitum either chow, a high-carbohydrate (HC), an intermediate-carbohydrate (IHC), a high-fat (HF), or an intermediate-fat (IHF) diet, all with equal protein content (g/kcal). The HF and IHF groups ate less food mass and, except for HC, all groups consumed similar kilocalories during the study. After 1 wk, we killed the animals and extracted total RNA from arcuate nucleus, cortex, and brown adipose tissue (BAT). Arcuate NPY mRNA in the HF group was significantly (P < 0.001) lower than in the HC and chow group. There were no differences between groups in NPY message in cortex or NPY protein in the paraventricular nucleus. BAT UCP message levels were significantly higher (P = 0.001) in the HF group. Thus HF compared with HC and chow diet reduces expression of NPY mRNA in hypothalamic nuclei and increases expression of BAT UCP message.

Adipose Tissue, Brown↗

PubMed1994

Factors affecting the ability of a high beta-galactosidase yogurt to enhance lactose absorption.

Lactose in yogurt is better absorbed by lactase-deficient subjects than is an equivalent quantity of lactose in milk, presumably because of the microbial activity of the beta-galactosidase present in yogurt. In this study, we describe a process that increases the beta-galactosidase of yogurt 5- to 6-fold and the ability of this high lactase yogurt to enhance lactose absorption in lactase-deficient subjects. These subjects ingested the yogurt meals after a 12-h fast, and lactose malabsorption was determined by measuring breath hydrogen. Breath hydrogen was reduced 39% following ingestion of high lactase yogurt from that after consumption of conventional yogurt, indicating that the high lactase yogurt enhanced lactose absorption. However, the reduction after high lactase yogurt was less than expected, given the 5- to 6-fold increment in beta-galactosidase measured in vitro. In vivo activity of beta-galactosidase requires that the enzyme resist acid denaturation in the stomach. The beta-galactosidase in high lactase yogurt was much less acid resistant than was the beta-galactosidase in conventional yogurt, and the relative inability of high lactase yogurt to enhance lactose absorption was likely due to the destruction of the beta-galactosidase in the stomach.

Absorption↗

PubMed1993

The effect of norbinaltorphimine, beta-funaltrexamine and naltrindole on NPY-induced feeding.

The non-selective opioid receptor antagonist naloxone decreases the robust feeding observed after i.c.v. injection of neuropeptide Y (NPY). In the present study we evaluated the effects of three selective opioid receptor antagonists on NPY-induced feeding. Graded doses of norbinaltorphimine (norBNI), beta-funaltrexamine (beta-FNA) and naltrindole (NTI), antagonists of the kappa, mu and delta receptors respectively, were preinjected (i.c.v.) in male rats prior to injection of 5 micrograms NPY (i.c.v.). Food intake was measured 1, 2 and 4 h post-NPY injection. Injection of beta-FNA and norBNI were most effective in reducing NPY-induced feeding, whereas NTI had little effect on NPY-induced feeding.

Animals↗

PubMed1992

Effect of yogurt on clindamycin-induced Clostridium difficile colitis in hamsters.

Yogurt exhibits in vitro bactericidal activity against a variety of pathogenic microorganisms, including Clostridium difficile. In the present studies, we tested whether yogurt ingestion could prevent or ameliorate antibiotic associated colitis in the clindamycin-treated hamster model. Male golden Syrian hamsters were given 5 mg/kg clindamycin subcutaneously 24 hr before and 6 hr following inoculation with 0.5 ml of less than 10, 10(3), 10(5), or 10(6) CFU/ml of C. difficile. Hamsters in the control group ingested chow and water ad libitum, whereas the experimental group ingested chow and a 1:1 (v/v) mixture of yogurt and water ad libitum, beginning 24 hr before the first injection of clindamycin and continuing throughout the course of the study. Animals were monitored for colonization with C. difficile, pathological evidence of colitis, and death. Mortality was 100% in yogurt-treated animals, and all animals showed histological changes of severe colitis. Fecal and intestinal segment cultures were positive for C. difficile in all animals. Thus, in the hamster model, we found no evidence to support the possible efficacy of yogurt in the prevention of C. difficile colitis.

Animals↗

PubMed1990

In vitro antibacterial effect of yogurt on Escherichia coli.

We investigated the bactericidal and bacteriostatic effects of yogurt on three strains of Escherichia coli: human toxigenic (078:H11), rabbit pathogenic (RDEC-1) and rabbit nonpathogenic [015:K14(L):H4]. Approximately 10(6) organisms were incubated in yogurt, milk, broth, and modifications of these materials. Aliquots were removed at various intervals and plated on MacConkey's agar for enumeration of E. coli. Yogurt was bactericidal (at least 5 log10 reduction in bacterial counts) to all three strains of E. coli with less than 10 CFU/ml remaining by 9 hr. In contrast, all three strains replicated rapidly in milk and broth, reaching maximum concentrations by 9 hr. The E. coli strains survived and multiplied in milk acidified to the same pH as the yogurt. Yogurt (native pH 4.1-4.4) in which the pH was brought up to and maintained at pH 5.5 or pH 7 for 8 hr was not bactericidal to E. coli. Heat-treated yogurt and the filtered supernatant of centrifuged yogurt (both containing no yogurt bacteria) were only bacteriostatic. We conclude that both live yogurt bacteria and a pH near 4.5 are necessary for the bactericidal activity of yogurt. The possibility that yogurt ingestion could protect against infection via other foods contaminated with pathogenic E. coli merits further in vivo investigation.

Animals↗