Particle Size, Surface Area, and Amorphous Content as Predictors of Solubility and Bioavailability for Five Commercial Sources of Ferric Orthophosphate in Ready-To-Eat Cereal.

Ferric orthophosphate (FePO₄) has had limited use as an iron fortificant in ready-to-eat (RTE) cereal because of its variable bioavailability, the mechanism of which is poorly understood. Even though FePO₄ has desirable sensory properties as compared to other affordable iron fortificants, few published studies have well-characterized its physicochemical properties. Semi-crystalline materials such as FePO₄ have varying degrees of molecular disorder, referred to as amorphous content, which is hypothesized to be an important factor in bioavailability.

Effects of two dietary fibers as part of ready-to-eat cereal (RTEC) breakfasts on perceived appetite and gut hormones in overweight women.

The effects of an enzyme-hydrolyzed arabinoxylan from wheat (AXOS) versus an intact arabinoxylan from flax (FLAX) added to a ready-to-eat cereal (RTEC) on the postprandial appetitive, hormonal, and metabolic responses in overweight women (BMI 25.0-29.9 kg/m2) were evaluated.

Leptin acts peripherally to limit meal-induced increases in plasma insulin concentrations in mice: a brief communication.

Leptin inhibits food intake and lowers plasma insulin concentrations. This study was designed to determine whether leptin acts independent of food-intake regulation to affect meal-induced increases in plasma insulin concentrations. Leptin-deficient, Lep(ob)/Lep(ob) mice were administered 1 microg leptin intracerebroventricularly (ICV) or intraperitoneally.

Desaturation of myristoyl-CoA to myristoleoyl-CoA by hen liver microsomal delta(9)-desaturase.

The desaturation of myristoyl-CoA to myristoleoyl-CoA was measured in microsomal preparations of hen liver. The desaturation was maximal at pH 7.4.

Direct desaturation of free myristic acid by hen liver microsomal Delta9-desaturase without prior activation to myristoyl-CoA derivative.

Direct desaturation of free myristic acid by hen liver microsomal Delta(9)-desaturase without prior activation to myristoyl-CoA by the addition of adenosine triphosphate (ATP) and CoA was observed when the incubation medium was mixed at mixing speeds of >250 rpm in the presence of fatty acid-binding proteins (FABP). Desaturation was linear with time and proportional to the microsomal protein concentration. Desaturation was maximal at pH 7.

Leptin administration normalizes insulin secretion from islets of Lep(ob)/Lep(ob) mice by food intake-dependent and -independent mechanisms.

Leptin-deficient Lep(ob)/Lep(ob) mice exhibit elevations in plasma insulin early in development. The present study tested the hypothesis that absence of leptin during neonatal development permanently programs islets from these mice to hypersecrete insulin. Administration of leptin for 8 days to young adult Lep(ob)/Lep(ob) mice normalized their food intake, plasma insulin concentration, and insulin secretion in response to glucose, acetylcholine, and leptin.

Leptin constrains phospholipase C-protein kinase C-induced insulin secretion via a phosphatidylinositol 3-kinase-dependent pathway.

Leptin-deficient Lep(ob)/Lep(ob)mice hypersecrete insulin in response to acetylcholine stimulation of the phospholipase C-protein kinase C (PLC-PKC) pathway, and leptin constrains this hypersecretion. Leptin has been reported to activate phosphatidylinositol 3-kinase (PI 3-K) and subsequently phosphodiesterase (PDE) to impair protein kinase A (PKA)-induced insulin secretion from cultured islets of neonatal rats. We determined if PKA-induced insulin secretion was also hyperresponsive in islets from Lep(ob)/Lep(ob)mice, and if leptin impaired this pathway in islets from these mice.

Intracerebroventricular leptin administration reduces food intake in pregnant and lactating mice.

Leptin acts within the hypothalamus to diminish food intake. During pregnancy and lactation, both circulating leptin concentrations and food intake are elevated, suggesting an ineffectiveness of leptin to reduce food intake in these mice. Thus, this study tested the ability of intracerebroventricular (ICV) leptin administration to alter food intake during pregnancy and lactation.

Leptin-deficient mice commence hypersecreting insulin in response to acetylcholine between 1 and 2 weeks of age.

Leptin-deficient Lep(ob)/Lep(ob)mice develop hyperinsulinemia early in life, before they begin to overeat or develop insulin resistance. Pancreatic islets from these young mice do not yet hypersecrete insulin in response to glucose, but they hyperrespond to acetylcholine. Islets from 4-day, and 1-, 2-, and 4-week-old mice were used in the present study to determine when leptin-deficient mice first hypersecrete insulin in response to acetylcholine.

Leptin rapidly inhibits hypothalamic neuropeptide Y secretion and stimulates corticotropin-releasing hormone secretion in adrenalectomized mice.

Leptin may rapidly inhibit food intake by altering the secretion of hypothalamic neuropeptides such as neuropeptide Y (NPY), a stimulator of food intake, and/or corticotropin-releasing hormone (CRH), an inhibitor of food intake. We measured concentrations of NPY and CRH in specific hypothalamic regions [i.e.

Leptin alters metabolic rates before acquisition of its anorectic effect in developing neonatal mice.

Leptin inhibits food intake and increases metabolic rates in adult mice. Neonatal mice need to maximize food intake and also maintain high thermoregulatory metabolic rates to optimize survival, suggesting that leptin may function differentially in neonatal versus adult animals. The efficacy of exogenous leptin to alter these two physiological functions during development was thus examined in C57BL/6J lean (+/+ or ob/+) and ob/ob (leptin-deficient) mice.

Neuropeptide Y and corticotropin-releasing hormone concentrations within specific hypothalamic regions of lean but not ob/ob mice respond to food-deprivation and refeeding.

Leptin is proposed to control food intake at least in part by regulating hypothalamic neuropeptide Y (NPY), a stimulator of food intake, and corticotropin-releasing hormone (CRH), an inhibitor of food intake. Ob/ob mice are leptin-deficient and would thus be expected to exhibit alterations in hypothalamic NPY and CRH. We therefore measured concentrations of NPY and CRH in discrete regions of the hypothalamus (i.

Leptin rapidly lowers food intake and elevates metabolic rates in lean and ob/ob mice.

Leptin, the ob gene product, is released from adipose tissue and likely acts in the central nervous system, particularly within the hypothalamus, to exert many of its effects. Obesity in C57BL/6J ob/ob mice is caused by a mutation in the ob gene resulting in a lack of functional leptin. In this study, we first compared effects of a single intracerebroventricular (ICV) injection of 3 pmol (50 ng) or 60 pmol (1 microg) leptin on food intake and oxygen consumption of lean and ob/ob mice deprived of food for 4 h during the 48-h period postinjection.

Leptin constrains acetylcholine-induced insulin secretion from pancreatic islets of ob/ob mice.

Hypersecretion of insulin from the pancreas is among the earliest detectable metabolic alterations in some genetically obese animals including the ob/ob mouse and in some obesity-prone humans. Since the primary cause of obesity in the ob/ob mouse is a lack of leptin due to a mutation in the ob gene, we tested the hypothesis that leptin targets a regulatory pathway in pancreatic islets to prevent hypersecretion of insulin. Insulin secretion is regulated by changes in blood glucose, as well as by peptides from the gastrointestinal tract and neurotransmitters that activate the pancreatic islet adenylyl cyclase (e.

Persistently enhanced sensitivity of pancreatic islets from ob/ob mice to PKC-stimulated insulin secretion.

Islets from 2-wk-old ob/ob and lean littermate mice were cultured for 4-12 days and then perifused or statically incubated to identify early-onset differences in their regulation of insulin secretion. Islets from these young ob/ob and lean mice increased insulin secretion similarly in response to glucose (10 or 20 mM), whereas responsiveness to glucose plus acetylcholine (10 microM) was greater in islets from ob/ob mice than lean mice. This phenotype-specific effect of acetylcholine was mimicked by phorbol 12-myristate 13-acetate (PMA, 100 nM), a protein kinase C (PKC) agonist, whereas prior downregulation of PKC abolished this phenotype-specific effect of acetylcholine.

Dexamethasone rapidly increases hypothalamic neuropeptide Y secretion in adrenalectomized ob/ob mice.

A single intracerebroventricular injection of dexamethasone (DEX) rapidly (within 30 min) suppresses brown adipose tissue thermogenesis and increases plasma insulin concentrations in adrenal-ectomized (ADX) ob/ob mice but not in ADX lean mice. Intracerebroventricular neuropeptide Y (NPY) administered intracerebroventricularly causes these same metabolic changes within 30 min in both ob/ob and lean ADX mice. We therefore hypothesized that DEX exerts these rapid-onset metabolic actions in ob/ob mice via a phenotype-specific enhancement of NPY secretion within the central nervous system.

Adrenalectomy reverses pre-existing obesity in adult genetically obese (ob/ob) mice.

Objective: To determine if adrenalectomy would reverse the pre-existing gross obesity, characteristic of adult genetically obese (ob/ob) mice.

Design: Adult (12 week old) female ob/ob mice were adrenalectomized and fed a stock diet for 6 or 14 weeks. They were housed at 23-25 degrees C or 33 degrees C.

A single intracerebroventricular injection of dexamethasone elevates food intake and plasma insulin and depresses metabolic rates in adrenalectomized obese (ob/ob) mice.

A single intracerebroventricular (ICV) injection of dexamethasone rapidly (within 30 min to 3 h) increases plasma insulin and suppresses oxygen consumption in adrenalectomized ob/ob mice with minimal effects in lean mice. Food intake of these adrenalectomized ob/ob mice was unaffected by ICV dexamethasone during these short-term studies. However, in a longer-term study with adrenalectomized gold thioglucose-lesioned obese mice, food intake increased fourfold 6-8 d after a single ICV injection of dexamethasone.

Consumption of a glucose diet enhances the sensitivity of pancreatic islets from adrenalectomized genetically obese (ob/ob) mice to glucose-induced insulin secretion.

Consumption of a glucose diet for 4 d markedly elevates plasma insulin concentrations in adrenalectomized ob/ob mice. The present study examined regulation of insulin secretion from perifused pancreatic islets of female adrenalectomized genetically obese (ob/ob) and lean mice fed a glucose diet for 4 d. These mice were fed a high carbohydrate commercial diet for 21 d, or the high carbohydrate commercial diet for 17 d and a purified high glucose diet for the last 4 d of the 21-d feeding period.

Enhanced sensitivity of pancreatic islets from preobese 2-week-old ob/ob mice to neurohormonal stimulation of insulin secretion.

Insulin secretion from perifused islets of preobese, 2-week-old, genetically obese (ob/ob) mice and their lean littermates was examined to identify early-onset abnormalities in regulation of insulin secretion by ob/ob mice. The ob/ob mice were slightly hyperinsulinemic (+20%) and hypoglycemic (-12%) at 2 weeks of age. Pancreatic islet size, DNA content, and insulin content were similar in ob/ob and lean mice.

Elevated neuronal c-Fos-like immunoreactivity and messenger ribonucleic acid (mRNA) in genetically obese (ob/ob) mice.

Adult genetically obese (ob/ob) mice display a number of metabolic alterations, the primary cause of which may be a defect in their central nervous system (CNS). The protein encoded by the protooncogene c-fos, c-Fos, functions as a nuclear transcription factor, and also serves as a marker of neuronal activity. The specific objectives of this study were (1) to use c-Fos immunohistochemistry to identify regions with altered neuronal activity in 6-7 week old male lean and ob/ob mice; (2) to examine c-fos relative mRNA abundance by northern blot analysis in brains of these mice and compare it with that of neuropeptide Y (NPY), a peptide well known to alter feeding and (3) determine changes in c-Fos immunoreactivity and mRNA caused by food deprivation.

Adrenalectomy suppresses insulin secretion from pancreatic islets of ob/ob mice.

The aim of this work was to examine effects of adrenalectomy and intracerebroventricular injection of dexamethasone on insulin secretion from pancreatic islets of ob/ob mice. Female ob/ob and lean mice fed a stock diet were adrenalectomized at 5 wk of age and studied at 8-9 wks of age. Removal of the adrenal glands from ob/ob mice fed a stock diet normalized their plasma insulin concentration, islet size, and essentially normalized insulin secretion from islets incubated in 10 mM glucose.

Corticotropin-releasing hormone decreases feeding, oxygen consumption and activity of genetically obese (ob/ob) and lean mice.

Acute effects of intracerebroventricularly administered corticotropin-releasing hormone (CRH) on deprivation-induced food intake, whole-body oxygen consumption, brown adipose tissue metabolism, and several locomotive behaviors were examined in 6- to 7-wk-old female genetically obese (ob/ob) and lean mice. Corticotropin-releasing hormone depressed food intake in a dose-dependent manner, with a tendency for greater suppression of intake in intact ob/ob mice than in lean mice. Adrenalectomy abolished this tendency for CRH to be more potent in ob/ob mice than in lean mice.

Type II glucocorticoid receptors in the CNS regulate metabolism in ob/ob mice independent of protein synthesis.

A single intracerebroventricular injection of dexamethasone rapidly (within 30 min) decreases brown adipose tissue thermogenesis by 25% as assessed by GDP binding and increases plasma insulin twofold in adrenalectomized ob/ob mice. The present study investigated the type of corticoid receptor(s) that mediate these effects and determined whether protein synthesis was necessary for expression of these glucocorticoid actions in ob/ob mice. Intracerebroventricular injection of aldosterone (a type I-corticoid receptor agonist) was ineffective in altering peripheral metabolism in adrenalectomized ob/ob mice, whereas RU-486 (a type II-corticoid receptor antagonist) abolished the effects of dexamethasone.

Threshold for glucose-stimulated insulin secretion in pancreatic islets of genetically obese (ob/ob) mice is abnormally low.

Pancreatic islets were isolated from 8-9-wk-old female genetically obese (ob/ob) and lean mice to determine the glucose threshold for insulin secretion, and to examine effects of acetylcholine on insulin secretion. Only equal-sized islets from ob/ob and lean mice were incubated to eliminate confounding effects of phenotypic differences in islet size. Even after this adjustment, islets from ob/ob mice still hypersecreted insulin in response to 20 mmol/L glucose.