Changes in Glucose Homeostasis after Roux-en-Y Gastric Bypass Surgery for Obesity at Day Three, Two Months, and One Year after Surgery: Role of Gut Peptides.
"Endocrine effects of gastric bypass (GBP) surgery for obesity on glucose homeostasis are not fully understood."
"Both enhanced insulin sensitivity and incretin hormones, such as GLP-1, contribute to the early control of glucose homeostasis. Progressively increasing postprandial levels of enteroglucagon (oxyntomodulin) and GLP-1 facilitate weight loss and enhance insulin effectiveness."
Serum bile acids are higher in humans with prior gastric bypass: potential contribution to improved glucose and lipid metabolism.
It has also been suggested that poor and slow bile acid secretion in obese people is responsible for poor GLP-1 secretions.
In this study the authors speculate that the higher concentration of blood bile acids is enforced by increased bile acid uptake by the ileum because it is moved closer to the entrance from the stomach.
"Post-GB anatomic or functional adaptive changes, including altered dietary patterns, intestinal motility, mucosal hyperplasia, or gut flora, could each contribute to increased postprandial bile acid absorption."
Sunday, 31 July 2011
liraglutide - new weight loss, GLP-1 agonist drug
The contribution of serotonin 5-HT2C and melanocortin-4 receptors to the satiety signaling of glucagon-like peptide 1 and liragultide, a glucagon-like peptide 1 receptor agonist, in mice.
"liraglutide, a GLP-1 receptor (GLP-1R) agonist, induces satiety."
" The serotonin 5-HT2C receptor (5-HT2CR) and melanoroctin-4 receptor (MC4R) are involved in the regulation of food intake."
The above study is able to show that the anorexia effects of GLP-1 is diminished in mice with 5-HT2C and MC4R receptor abnormalities, which would suggest some of the downstream effects of GLP-1 binding acts on those receptors.
However, strangely, the new drug liraglutide is still able to mimic the anorexia effects of GLP-1 in mice with those same receptor abnormalities. Clearly liraglutide is doing more than what it says on the tin.
Comparative Effects of the Long-Acting GLP-1 Receptor Ligands, Liraglutide and Exendin-4, on Food Intake and Body Weight Suppression in Rats.
"liraglutide reduced 24 and 48 h body weight in nonobese, chow-maintained rats"
"Chow intake and body weight suppression by liraglutide were of greater magnitude and shorter latency following intraperitoneal compared to subcutaneous delivery,"
"Both drugs regimens yielded marked weight loss over the 7-day period. The weight loss effect of liraglutide was achieved in the first 2 days and remained stable for the duration of the experiment; weight loss with exendin-4 appeared more linear over the 7-day period."
Liraglutide Prevents Hypoadiponectinemia-Induced Insulin Resistance and Alterations of Gene Expression Involved in Glucose and Lipid Metabolism.
"Administration of liraglutide prevented hypoadiponectinemia-induced increases in plasma insulin, free fatty acids, triglycerides and total cholesterol. Liraglutide also attenuated hypoadiponectinemia-induced deterioration in peripheral and hepatic insulin sensitivity and alterations in key regulatory factors implicated in glucose and lipid metabolism. "
"These findings demonstrated for the first time that liraglutide could be used to rescue insulin resistance induced by hypoadiponectinemia and HFD via regulating gene and protein expression involved in glucose and lipid metabolism."
Wow, this drug sounds too good to be true.........
"liraglutide, a GLP-1 receptor (GLP-1R) agonist, induces satiety."
" The serotonin 5-HT2C receptor (5-HT2CR) and melanoroctin-4 receptor (MC4R) are involved in the regulation of food intake."
The above study is able to show that the anorexia effects of GLP-1 is diminished in mice with 5-HT2C and MC4R receptor abnormalities, which would suggest some of the downstream effects of GLP-1 binding acts on those receptors.
However, strangely, the new drug liraglutide is still able to mimic the anorexia effects of GLP-1 in mice with those same receptor abnormalities. Clearly liraglutide is doing more than what it says on the tin.
Comparative Effects of the Long-Acting GLP-1 Receptor Ligands, Liraglutide and Exendin-4, on Food Intake and Body Weight Suppression in Rats.
"liraglutide reduced 24 and 48 h body weight in nonobese, chow-maintained rats"
"Chow intake and body weight suppression by liraglutide were of greater magnitude and shorter latency following intraperitoneal compared to subcutaneous delivery,"
"Both drugs regimens yielded marked weight loss over the 7-day period. The weight loss effect of liraglutide was achieved in the first 2 days and remained stable for the duration of the experiment; weight loss with exendin-4 appeared more linear over the 7-day period."
Liraglutide Prevents Hypoadiponectinemia-Induced Insulin Resistance and Alterations of Gene Expression Involved in Glucose and Lipid Metabolism.
"Administration of liraglutide prevented hypoadiponectinemia-induced increases in plasma insulin, free fatty acids, triglycerides and total cholesterol. Liraglutide also attenuated hypoadiponectinemia-induced deterioration in peripheral and hepatic insulin sensitivity and alterations in key regulatory factors implicated in glucose and lipid metabolism. "
"These findings demonstrated for the first time that liraglutide could be used to rescue insulin resistance induced by hypoadiponectinemia and HFD via regulating gene and protein expression involved in glucose and lipid metabolism."
Wow, this drug sounds too good to be true.........
Insulin and Leptin is needed for Fertility
Direct insulin and leptin action on pro-opiomelanocortin neurons is required for normal glucose homeostasis and fertility.
" the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established"
"Here, we show that mice lacking both leptin and insulin receptors in POMC neurons display systemic insulin resistance, which is distinct from the single deletion of either receptor."
"We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function"
" the physiological significance of concomitant leptin and insulin action on POMC neurons remains to be established"
"Here, we show that mice lacking both leptin and insulin receptors in POMC neurons display systemic insulin resistance, which is distinct from the single deletion of either receptor."
"We conclude that direct action of insulin and leptin on POMC neurons is required to maintain normal glucose homeostasis and reproductive function"
Friday, 29 July 2011
Smoking ( Nicotine ) really does help you stay thin
Nicotine decreases food intake through activation of POMC neurons.
"This study demonstrates that nicotine decreases food intake and body weight by influencing the hypothalamic melanocortin system and identifies critical molecular and synaptic mechanisms involved in nicotine-induced decreases in appetite."
"This study demonstrates that nicotine decreases food intake and body weight by influencing the hypothalamic melanocortin system and identifies critical molecular and synaptic mechanisms involved in nicotine-induced decreases in appetite."
Carbs may sabotage your GLP-1 response
The effect on glucagon, glucagon-like peptide-1, total and acyl-ghrelin of dietary fats ingested with and without potato
In this study we see that, lard produces a strong and somewhat delayed spike in GLP-1, you get the spike about 2.5hours after ingestion.
Olive oil gives you a GLP-1 increase that happens sooner than lard but doesnt reach as high a concentration, the increase also remains elevated for longer than lard.
Ingestion of carbs ( potato ) with the fats listed above completely blunts up the GLP-1 response.
In this study we see that, lard produces a strong and somewhat delayed spike in GLP-1, you get the spike about 2.5hours after ingestion.
Olive oil gives you a GLP-1 increase that happens sooner than lard but doesnt reach as high a concentration, the increase also remains elevated for longer than lard.
Ingestion of carbs ( potato ) with the fats listed above completely blunts up the GLP-1 response.
Glucose sensing by POMC neurons regulates glucose homeostasis and is impaired in obesity
Funny Stuff
" We also found that glucose sensing by POMC neurons became defective in obese mice on a high-fat diet, suggesting that loss of glucose sensing by neurons has a role in the development of type 2 diabetes."
"The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production."
"UCP2 negatively regulates glucose sensing in POMC neurons. We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing,"
" We also found that glucose sensing by POMC neurons became defective in obese mice on a high-fat diet, suggesting that loss of glucose sensing by neurons has a role in the development of type 2 diabetes."
"The mechanism for obesity-induced loss of glucose sensing in POMC neurons involves uncoupling protein 2 (UCP2), a mitochondrial protein that impairs glucose-stimulated ATP production."
"UCP2 negatively regulates glucose sensing in POMC neurons. We found that genetic deletion of Ucp2 prevents obesity-induced loss of glucose sensing,"
Thursday, 28 July 2011
Over-eat but dont get fat?
ATP-Sensitive Potassium Channel-Deficient Mice Show Hyperphagia but Are Resistant to Obesity.
"Body weight homeostasis is maintained through the balance between energy expenditure and energy intake, and these processes are controlled in the hypothalamus - the center for body weight regulation."
"When anorexigenic peptide is elevated, melanocortin receptor 3/4 in the paraventricular nucleus of the hypothalamus is activated and satiation and thermogenesis are induced. Increased orexigenic peptide activates the Y1/5 receptor in the paraventricular nucleus of the hypothalamus, induces a sense of hunger, and halts thermogenesis"
"This study demonstrated that Kir6.2-deficient mice showed increased hypothalamic NPY expression accompanied with increased caloric intake, decreased visceral fat mass, and resistance to the induction of obesity by a high fat diet compared to the levels in C57BL/6 mice."
"Body weight homeostasis is maintained through the balance between energy expenditure and energy intake, and these processes are controlled in the hypothalamus - the center for body weight regulation."
"When anorexigenic peptide is elevated, melanocortin receptor 3/4 in the paraventricular nucleus of the hypothalamus is activated and satiation and thermogenesis are induced. Increased orexigenic peptide activates the Y1/5 receptor in the paraventricular nucleus of the hypothalamus, induces a sense of hunger, and halts thermogenesis"
"This study demonstrated that Kir6.2-deficient mice showed increased hypothalamic NPY expression accompanied with increased caloric intake, decreased visceral fat mass, and resistance to the induction of obesity by a high fat diet compared to the levels in C57BL/6 mice."
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