Sunday, 31 July 2011

Gastric Bypass Surgery And Gut Peptides

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."

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.........

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"

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."

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.

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,"

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."

Glucose regulates the effects of leptin on hypothalamic POMC neurons.

The body works on thresholds.

Some may not be better than none.

More may not be better than some.

Insulin resistance is a cellular antioxidant defense mechanism

Theres no ends to wierd stuff you can find when you dig deep enough in pubmed.

Metformin increases leptin sensitivity

The anorexigenic effects of metformin involve increases in hypothalamic leptin receptor expression.

"These data identify the hypothalamic ObRb as a gene modulated after metformin treatment and suggest that the anorectic effects of the drug are potentially mediated via an increase in the central sensitivity to leptin."

Artificial sweeteners

Effects of carbohydrate sugars and artificial sweeteners on appetite and the secretion of gastrointestinal satiety peptides.

Study showing that artificial sweeteners have no effect on your physiological hormones in your gut, contrary to popular belief.

Think your in control? Well, Your not

Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite.

This study was a true eye opener for me. The idea of "free will" and "choice" is thrown into complete disarray here.

Basically, what this study shows is that the unconcious part of your brain will use dopamine signalling and other feel good reward chemistry in your brain in an attempt to control your behaviour in such a way so that you do what *it* thinks is ultimately best for your survival or prosperity.

Notice however, that whether or not the action your unconciousness is encouraging you to do REALLY IS in your best benefits is a different matter. That is to say, your unconciousness is not always RIGHT.

Free will and choice can only exsist in a situation where the outcomes of any of your actions are negligible to your survival and/or prosperity.

Glucagon-like peptide 1 stimulates hypothalamic proopiomelanocortin neurons.

Interesting study

Friday, 15 July 2011

Adipocyte Apoptosis and Resveratrol

Effect of resveratrol on fat mobilization.

"Moreover, dietary supplementation of aged ovariectomized rats with a combination of resveratrol and vitamin D, quercetin, and genistein not only decreased weight gain but also inhibited bone loss."

"Combining several phytochemicals, including resveratrol, or using them as templates for synthesizing new drugs, provides a large potential for using phytochemicals to target adipocyte adipogenesis, apoptosis, and lipolysis."

Enhanced inhibition of adipogenesis and induction of apoptosis in 3T3-L1 adipocytes with combinations of resveratrol and quercetin.

" Taken together, our data indicate that combinations of resveratrol and quercetin can exert potential anti-obesity effects by inhibiting differentiation of preadipocytes and inducing apoptosis of mature adipocytes."

Thursday, 14 July 2011

More Neuropeptide Y stuff

Short-term cold exposure may cause a local decrease of neuropeptide Y in the rat hypothalamus.

Leptin inhibits hypothalamic Npy and Agrp gene expression via a mechanism that requires phosphatidylinositol 3-OH-kinase signaling.

NPY receptors as drug targets for the central regulation of body weight.

Hyperprolactinemia suppresses the luteinizing hormone responses to N-methyl-D-aspartate, epinephrine, and neuropeptide-Y in male rats.

Neuropeptide Y in relation to carbohydrate intake, corticosterone and dietary obesity.

Neuropeptide Y projection from arcuate nucleus to parvocellular division of paraventricular nucleus: specific relation to the ingestion of carbohydrate.

NPY in the coordination of bone mass to body weight

Neuropeptide Y knockout mice reveal a central role of NPY in the coordination of bone mass to body weight.

Basically, high NPY = low bone density, and low NPY = high bone mass

NPY is another starvation hormone, it basically tells your body that your starving and that all ingested calories should go towards storage.

Stopping Coconut Oil for a Bit - Mind in OVERDRIVE

Been taking 40g coconut oil in mornings last few days and ive noticed ever increaseing duration in the nausea it produces afterwards,

Its got so bad that my thoughts are just racing like mad constantly and its impacting my ability to sleep, been waking up at 3am last few nights and this morning I wasnt even able to get back to sleep.

Whats interesting is that I dont even feel that tired, I just have this constant hyper caffeine high.

Will give it a rest for a few days.

Wednesday, 13 July 2011

Ketone bodies modulates body weight and hepatic insulin sensitivity

Central infusion of ketone bodies modulates body weight and hepatic insulin sensitivity by modifying hypothalamic leptin and insulin signaling pathways in type 2 diabetic rat

"In conclusion, mild ketosis by central infusion of ketones improves energy and glucose metabolism through the potentiation of leptin and insulin signaling in the hypothalamus of diabetic rats."

Obesity and more.....

Well it seems as ever you learn far more from reading the comments section of aritcles than the actual articles themselves.

This post is just a summation of some interesting information and to serve as a bookmark.

Brain dopamine and obesity.

"The availability of dopamine D2 receptor was decreased in obese individuals in proportion to their BMI."

Dopamine signalling is an important way for your brain to decide if ingested calories go towards energy and reproduction or if its just going to be stored in fat cells. There is some evidence that dopamine agonists ( i.e. dopamine receptor activators ) can help with keeping metabolsim high and helping partition calories towards energy production instead of storage. Drugs such as Bromocriptine and Cabergoline and Pergolide have been implicated.

Activation of dopamine D2 receptors simultaneously ameliorates various metabolic features of obese women.

"Thus these results imply that short-term bromocriptine treatment ameliorates various components of the metabolic syndrome while it shifts energy balance away from lipogenesis in obese humans."

Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics.

Interesting paper by Lustig.

Attenuated GLP-1 secretion in obesity: cause or consequence?

"Postprandial GLP-1 secretion in response to oral carbohydrate is considerably attenuated in obese subjects. The cause of this attenuation of GLP-1 secretion is not known although we suggest that both this fall and the overall reduction in GLP-1 values in obese subjects may be related to an increase in plasma non-esterified fatty acids."

Thanks to Itsthewoo for pointing this paper out.

Diet high in oat β-glucan activates the gut-hypothalamic (PYY(3-36) -NPY) axis and increases satiety in diet-induced obesity in mice

Just throwing it out there. Will read up on it more when I get time.

Saturday, 2 July 2011

Another take at muscle building

I had this idea the other day that I may have overlooked in my research on muscle building. The golden rule of biology is that, in all circumstances, cells always seek to adapt to thier environment in such a way so as to maintain homeostasis with that environment.

In light of this, it may not be wise to complete strength training sets to failure or near failure. Going to failure surely creates an environment for the cell that ultimately favours aerobic respiration, i.e, high endurance. So this is what the cell adapts to, endurance, i.e. lots of type I fibres with densely packed mitochondria.

It could therefore be alot more beneifical to not go anywhere near failure when performing a set, giving us the stimulation for type II fibre hypertrophy WITHOUT the stimulation for many high endurance type I fibres.

This is just another theory, I will test it on myself in the coming months by only performing enough reps in a set to take me to about ~70% close to failure.

For example, if for a given weight I can only perform 12 reps of bicep curls before I hit failure, ( so I cannot complete the 13th rep ), then I will pick that weight and only do sets of 8 reps.

To compensate for the reduced volume this would bring ( and we know that volume is one of the important things for building muscle ), I will increase the total number of sets I do for a given exercise , 1-2 or something, depending on how I feel the muscle is coping.