All Relations between feeding and insulin

Publication Sentence Publish Date Extraction Date Species
J J Wilkes, L E Nag. Chronic ethanol feeding impairs glucose tolerance but does not produce skeletal muscle insulin resistance in rat epitrochlearis muscle. Alcoholism, clinical and experimental research. vol 20. issue 6. 1997-02-21. PMID:8892521. these data demonstrate that chronic ethanol feeding impairs glucose tolerance; impaired glucose tolerance was associated with an inability to maintain plasma insulin levels, rather than the development of skeletal muscle insulin resistance. 1997-02-21 2023-08-12 rat
A E Meinders, A C Toornvliet, H Pij. Leptin. The Netherlands journal of medicine. vol 49. issue 6. 1997-02-20. PMID:8990865. a feedback inhibition of leptin on hypothalamic neuropeptide y (ny) production is postulated, as hypothalamic ny concentrations are increased in ob/ob mice and ny induces food intake, insulin secretion and autonomic nervous system activity. 1997-02-20 2023-08-12 mouse
X Remesar, I Rafecas, J A Fernández-López, M Aleman. Is leptin an insulin counter-regulatory hormone? FEBS letters. vol 402. issue 1. 1997-02-20. PMID:9013847. leptin may be, essentially, a counter-regulatory hormone limiting the insulin drive to store energy in the form of fat, its effects reaching from a decrease in food intake to lower insulin secretion and increased resistance to insulin and lower glucose uptake and fat synthesis by wat. 1997-02-20 2023-08-12 Not clear
E Nisoli, V Garosi, J E Blundell, M O Carrub. Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia. Pharmacology, biochemistry, and behavior. vol 54. issue 2. 1997-02-12. PMID:8743603. the role of beta-adrenoreceptors in modulating feeding in glucoprivation- and lipoprivation-induced hyperphagias was studied in rats by measuring the efficacy of the selective beta2-adrenoreceptor agonist salbutamol to antagonize the hyperphagic response induced by injection of 2-deoxy-d-glucose (2-dg), insulin, or sodium mercaptoacetate (ma). 1997-02-12 2023-08-12 rat
E Nisoli, V Garosi, J E Blundell, M O Carrub. Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia. Pharmacology, biochemistry, and behavior. vol 54. issue 2. 1997-02-12. PMID:8743603. we found that salbutamol dose-dependently antagonized both the insulin- and ma-induced hyperphagia, with reductions in food intake up to 100% compared with rats treated with insulin or ma alone. 1997-02-12 2023-08-12 rat
E Nisoli, V Garosi, J E Blundell, M O Carrub. Salbutamol antagonizes insulin- and sodium mercaptoacetate-induced but not 2-deoxy-D-glucose-induced hyperphagia. Pharmacology, biochemistry, and behavior. vol 54. issue 2. 1997-02-12. PMID:8743603. the present results support the previously proposed notion that there are different neuronal or humoral circuits underlying the hyperphagic responses to the metabolic stimuli induced by glucoprivation (i.e., 2-dg and insulin administration), and they extend our knowledge on the effects of salbutamol on glucoprivic and lipoprivic control of feeding. 1997-02-12 2023-08-12 rat
S Choi, C Horsley, S Aguila, M F Dallma. The hypothalamic ventromedial nuclei couple activity in the hypothalamo-pituitary-adrenal axis to the morning fed or fasted state. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 16. issue 24. 1997-02-06. PMID:8987842. the hypothalamic ventromedial nuclei (vmn) appear to signal satiety; lesions result in increased food intake, obesity, and elevated basal insulin and corticosteroids. 1997-02-06 2023-08-12 rat
M W Schwartz, R J Seele. The new biology of body weight regulation. Journal of the American Dietetic Association. vol 97. issue 1. 1997-02-05. PMID:8990418. these include the circulating signals, leptin (the hormone encoded by the ob gene that is secreted by fat cells) and the pancreatic hormone insulin; and brain peptides such as neuropeptide y, which is released from nerve terminals in the hypothalamus to elicit changes in feeding behavior and energy expenditure that mediate adaptive changes in energy balance. 1997-02-05 2023-08-12 human
B Ozel, J F Youngren, J K Kim, I D Goldfine, C K Sung, J H You. The development of insulin resistance with high fat feeding in rats does not involve either decreased insulin receptor tyrosine kinase activity or membrane glycoprotein PC-1. Biochemical and molecular medicine. vol 59. issue 2. 1997-02-04. PMID:8986641. the development of insulin resistance with high fat feeding in rats does not involve either decreased insulin receptor tyrosine kinase activity or membrane glycoprotein pc-1. 1997-02-04 2023-08-12 rat
B Ozel, J F Youngren, J K Kim, I D Goldfine, C K Sung, J H You. The development of insulin resistance with high fat feeding in rats does not involve either decreased insulin receptor tyrosine kinase activity or membrane glycoprotein PC-1. Biochemical and molecular medicine. vol 59. issue 2. 1997-02-04. PMID:8986641. in the present study, we examined whether either insulin receptor function or pc-1 activity was altered during the development of insulin resistance that occurs with high fat feeding in normal rats. 1997-02-04 2023-08-12 rat
B Ozel, J F Youngren, J K Kim, I D Goldfine, C K Sung, J H You. The development of insulin resistance with high fat feeding in rats does not involve either decreased insulin receptor tyrosine kinase activity or membrane glycoprotein PC-1. Biochemical and molecular medicine. vol 59. issue 2. 1997-02-04. PMID:8986641. together, these data indicate that neither defects in insulin receptor function nor elevated pc-1 activities are involved in the development of insulin resistance in rats with high fat feeding, and the insulin resistance induced with high fat feeding is likely due to postreceptor defects in skeletal muscle. 1997-02-04 2023-08-12 rat
T C Ballard, A Farag, G D Branum, O E Akwari, E C Opar. Effect of L-glutamine supplementation on impaired glucose regulation during intravenous lipid administration. Nutrition (Burbank, Los Angeles County, Calif.). vol 12. issue 5. 1997-01-23. PMID:8875520. however, addition of l-glutamine to the high-dose lipid infusion with chow feeding prevented changes in plasma glucose, insulin levels, and ffa but not triglyceride levels. 1997-01-23 2023-08-12 rat
T C Ballard, A Farag, G D Branum, O E Akwari, E C Opar. Effect of L-glutamine supplementation on impaired glucose regulation during intravenous lipid administration. Nutrition (Burbank, Los Angeles County, Calif.). vol 12. issue 5. 1997-01-23. PMID:8875520. also, glutamine but not alanine supplementation in intralipid infused rats without chow feeding prevented changes in plasma glucose, insulin, and malondialdehyde levels. 1997-01-23 2023-08-12 rat
Y B Lombardo, S Drago, A Chicco, P Fainstein-Day, R Gutman, J J Gagliardino, C L Gomez Dum. Long-term administration of a sucrose-rich diet to normal rats: relationship between metabolic and hormonal profiles and morphological changes in the endocrine pancreas. Metabolism: clinical and experimental. vol 45. issue 12. 1997-01-22. PMID:8969287. we found that long-term feeding with a srd resulted in a steady state of hypertriglyceridemia and hyperglycemia in which insulin levels remained unchanged and unable to compensate for the increased demands of the developing metabolic changes. 1997-01-22 2023-08-12 human
Y B Lombardo, S Drago, A Chicco, P Fainstein-Day, R Gutman, J J Gagliardino, C L Gomez Dum. Long-term administration of a sucrose-rich diet to normal rats: relationship between metabolic and hormonal profiles and morphological changes in the endocrine pancreas. Metabolism: clinical and experimental. vol 45. issue 12. 1997-01-22. PMID:8969287. it may therefore be postulated that the newly emerged b-cell mass has some sort of derangement with the increased insulin demand resulting from insulin resistance induced by the long-term srd feeding. 1997-01-22 2023-08-12 human
Y B Lombardo, S Drago, A Chicco, P Fainstein-Day, R Gutman, J J Gagliardino, C L Gomez Dum. Long-term administration of a sucrose-rich diet to normal rats: relationship between metabolic and hormonal profiles and morphological changes in the endocrine pancreas. Metabolism: clinical and experimental. vol 45. issue 12. 1997-01-22. PMID:8969287. thus, feeding a srd to normal rats may prove to be an attractive animal model for studying the role of environmental nutritional factors in the unsettled issue of the relationship between insulin resistance and relative insulin deficiency. 1997-01-22 2023-08-12 human
S Ikemoto, M Takahashi, N Tsunoda, K Maruyama, H Itakura, O Ezak. High-fat diet-induced hyperglycemia and obesity in mice: differential effects of dietary oils. Metabolism: clinical and experimental. vol 45. issue 12. 1997-01-22. PMID:8969289. these data indicate that (1) fasting blood insulin levels vary among fat subtypes, and a higher fasting blood insulin level in palm oil-fed mice may explain their better glycemic control irrespective of their marked obesity; (2) a favorable glucose response induced by fish oil feeding may be mediated by a decrease of body weight; and (3) obesity and a higher intake of linoleic acid are independent risk factors for dysregulation of glucose tolerance. 1997-01-22 2023-08-12 mouse
P Holtenius, G Olsson, M Emanuelson, H Wiktorsso. Effects of different energy levels, concentrate/forage ratios and lipid supplementation to the diet on the adaptation of the energy metabolism at calving in dairy cows. Zentralblatt fur Veterinarmedizin. Reihe A. vol 43. issue 7. 1997-01-21. PMID:8921729. high intensity feeding (200 mj me and 50% concentrates) resulted in high basal serum insulin levels. 1997-01-21 2023-08-12 Not clear
J L Marks, K Waite, L Davie. Intracerebroventricular neuropeptide Y produces hyperinsulinemia in the presence and absence of food. Physiology & behavior. vol 60. issue 3. 1997-01-16. PMID:8873237. we concluded that icv neuropeptide y can stimulate insulin secretion even at low doses and this response does not completely depend on food intake. 1997-01-16 2023-08-12 rat
P Muzzin, R C Eisensmith, K C Copeland, S L Wo. Correction of obesity and diabetes in genetically obese mice by leptin gene therapy. Proceedings of the National Academy of Sciences of the United States of America. vol 93. issue 25. 1997-01-15. PMID:8962136. treatment resulted in dramatic reductions in both food intake and body weight, as well as the normalization of serum insulin levels and glucose tolerance. 1997-01-15 2023-08-12 mouse