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Nunez Ea1997Biological complexity is under the ‘strange attraction’of non-esterified fatty acids.
This article is composed of multiple excerpts to result in tone and content shifts and reference numbering that may be out of order.
Physical activity, like the previously mentioned resistance work, is crucial to the maintenance of lean muscle, as well (41). Glutamine (3 to 5 g), alpha ketoglutaric acid (2 g), and a mix of branched-chain amino acids (2 g) block cortisol secretions and promote protein synthesis to boost immune function and immediate tissue recovery, including muscle anabolism.
Once the targeted fat mass is reached, though, go back to consuming high-glycemic-index carbohydrates and high-biological-value protein immediately after the training session to optimize strength and muscle results. Elsevier Medical Journal Manuscript: Paradigm shift redefining molecular, metabolic and structural events in Alzheimer’s disease involves a proposed contribution by transition metals. It's a scientific fact that grass-fed poultry, pork and beef are far richer in nutritious value than commercially fed livestock. Because meat from grass-fed animals is lower in fat than meat from grain-fed animals, it is also lower in calories.
Meat from grass-fed animals has two to four times more omega-3 fatty acids than meat from grain-fed animals. In addition to being higher in omega-3s and CLA, meat from grassfed animals is also higher in vitamin E.
We would be happy to talk to you about the benefits that grass-fed farms and ranches like Willow Creek Ranch have to offer consumers, and people concerned about their health and the health of the land.
Bringing you Wisdom, Inspiration, entertainment and original creations that will brighten up your day. Did you know that more than 90 percent of male infertility cases are due to low sperm counts, poor sperm quality or both? Pomegranates are rich in an antioxidant that help to reduce a chemical found in sperm called malondialdehyde, which destroys sperm.
ONE DAY I DECIDED TO QUIT I quit my job, my relationship , my spirituality… I wanted to quit my life.
This man wanted to know why his wife was so tired every evening, so he spied on her for one day. This is a short movie from Japan which brings the awareness and answers, to the following question: “Who carries a heavier load? An 80 year old man was sitting on the sofa in his house along with his 45 years old highly educated son. Variation in free fatty acids (?) and insulin (0) concentrations in response to meals in healthy people (upper panel, reprinted from Frayn KN, 1998) [6] and fatty acid levels in mild essential hypertensive patients (---) and normotensive control subjects (——) (lower panel, reprinted from Singer P et al.
Insulin signaling pathway for glucose uptake stimulation (Reprinted from Frosig and Richter, 2009) [42].
Palmitate acutely stimulates AMPK and Akt phosphorylation in a time- and dose-dependent manner [41]. PA-induced glucose uptake is decreased when Akt activity is blocked by an Akt inhibitor (left panel) or RNAi (right panel) [41].
PA-induced glucose uptake and Akt phosphorylation is decreased when AMPK activity is reduced by an AMPK inhibitor (left panel) or AMPK dominant-negative construct (right panel) [41]. PI3K-specific inhibition abolishes PA-induced glucose uptake and phosphorylation of Akt and AMPK [41]. IntroductionObesity-driven type II diabetes mellitus has become a major crisis in modern societies. With exercise calories are expended to allow greater caloric intake for the purpose of improved nutrient ingestion, ultimately allowing more leeway when it comes to desired high-glycemic-index and fatty foods. Age-related muscle loss, as we’ve seen, is caused by a number of factors: insulin resistance, a lack of nutrient building blocks and co-factors from the diet, and an elevation in NF-kappa-B. Antioxidant needs increase with the onset of a more active lifestyle, and Ageless Performance accommodates for this demand, too. Thermogenic-related calorie losses can continue indefinitely long after exercise is terminated.
The immediate introduction of high-glycemic-index food after exercise puts out the thermogenic fire by raising insulin levels. Taking this multiple-aminoacid combination immediately after a workout supports health and maximizes fat loss by allowing serum fatty acids to maintain thermogenesis in the on position. Getting all of these strategies into your program will result in profound changes in your metabolic status quickly. Researcher Tilak Dhiman from Utah State University estimates that you may be able to lower your risk of cancer simply by eating the following grassfed products each day: one glass of whole milk, one ounce of cheese, and one serving of meat.
This graph below shows vitamin E levels in meat from: 1) feedlot cattle, 2) feedlot cattle given high doses of synthetic vitamin E (1,000 IU per day), and 3) cattle raised on fresh pasture with no added supplements. There are many things you can do to improve your sperm volume, and diet is definitely one of the most important things.
Dark chocolate contains L-Arginine HCL, an amino acid that doubles male sperm count and semen volume.
Pumpkin seeds are also loaded with omega-3 fatty acids, which stimulate blood flow to reproductive organs and improve it’s function. Garlic also provides the body with selenium and vitamin B6 which are responsible for the mechanism of healthy sperm production. Drinking pomegranate juice can help the body to get rid of free radicals and also in improve the quality of the sperms. Kuo, 2005The G-protein coupled receptor, GPR84 regulates IL-4 production by T lymphocytes in response to CD3 crosslinking. Insulin, remember, sweeps substrates like glucose, amino acids, and free fatty acids from the blood and into storage. However, maximum glycogen stores, muscle building, and strength aren’t possible applying this regimen all the time. The greater the fat content, the greater the number of calories.) As an example, a 6-ounce steak from a grass-finished steer can have 100 fewer calories than a 6-ounce steak from a grain-fed steer. You would have to eat five times that amount of grain-fed meat and dairy products to get the same level of protection. The meat from the pastured cattle is four times higher in vitamin E than the meat from the feedlot cattle and, interestingly, almost twice as high as the meat from the feedlot cattle given vitamin E supplements.
These foods have the power to improve your fertility levels, increase sperm count and motility.
L-arginine is also known to improve the dilation of blood vessels, which increases blood flow to male reproductive organs. To increase your sperm count, production, and motility, make sure you’re eating lots of dark green veggies. These essential fatty acids can improve blood flow to male reproductive organs and increase sperm count.
In the case of Chinese adult diabetic patients, diabetes is also significantly associated with obesity [2]. A deficiency of exercise or general physical activity also plays a significant role in age-related muscle atrophy. For this reason, to optimize fat-loss endeavors, you should wait 20 to 30 minutes after exercise before high-glycemic-index foods are consumed. If you eat a typical amount of beef (66.5 pounds a year), switching to lean grassfed beef will save you 17,733 calories a yeara€”without requiring any willpower or change in your eating habits. People who have ample amounts of omega-3s in their diet are less likely to have high blood pressure or an irregular heartbeat.
Previous investigations have focused on looking for obesity-related factors that cause insulin resistance, the failure of the body to respond to insulin, which is the hallmark of type II diabetes.

The abnormal plasma fatty acid metabolism associated with diabetes mellitus [3], and the high level of obesity-related plasma free fatty acids (FFAs, also known as non-esterified fatty acids, NEFA) have been identified since the 1950s as major risk factors for insulin resistance. Of course, as we’ve seen, this delay strategy increases the exposure to cortisol (a stress hormone produced during prolonged exercise) and reduces the potential for muscle and glycogen restoration.
If all Americans switched to grassfed meat, our national epidemic of obesity might diminish. Natural fatty acids are carboxylic acids with saturated or unsaturated aliphatic tails which have an even number of carbon atoms from 4 to 28. To counter this problem I run for 30 minutes or so in the morning and then work out in the late afternoon with weights for about 30 to 40 minutes.
People with a diet rich in omega-3s are less likely to suffer from depression, schizophrenia, attention deficit disorder (hyperactivity), or Alzheimer's disease.
When they are not incorporated into other compounds, like triglyceride or phospholipids, they are known as "free" fatty acids. It has been estimated that only 40 percent of Americans consume an adequate supply of omega-3 fatty acids. When metabolized, fatty acids yield a large quantity of ATP, and thus represent an important fuel for the body, particularly for heart and skeletal muscle. They are not only essential dietary nutrients, but also function in many cellular events by activating nuclear receptors, such as the peroxisome proliferator-activated receptors (PPARs), and fatty acid binding proteins (FABPs).How FFAs induce insulin resistance is not a novel topic in pathological studies on obesity-associated type II diabetes. Kuwahara, 2006Short-chain fatty acid receptor, GPR43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine.
Switching to the meat, milk, and dairy products of grass-fed animals is one way to restore this vital nutrient to your diet.
Many efforts have been made to uncover the underlying molecular mechanisms, but they remain elusive. Uejima, 2003Free fatty acids regulate insulin secretion from pancreatic ? cells through GPR40. It seems that FFA-induced insulin resistance occurs not via a single pathway but rather via a complicated network of pathways in organs, tissues, and cells.
Acute cellular responses to Free Fatty AcidsMajor investigatons of the mechanisms of extra FFA-induced insulin resistance have focused on the chronic effects of FFAs. However, plasma FFA concentrations are not consistent and vary widely from hour to hour, displaying waves according to nutritional state and the presence of regulators including hormones (Figure 1). Such plasma FFA fluctuations also occur in people with metabolic disorders, but display a different pattern.
In mild essential hypertensive patients, the plasma FFA concentrations at 3 and 4 h after a meal are significantly higher than that in healthy people (Figure 1, lower panel) [5]. 1985) [5].Previous works have reported that FFAs are able to acutely induce several cellular events in various tissues.
For example, FFAs can stimulate insulin secretion in pancreatic ?-cells [7, 8], leptin secretion in adipocytes [9], and glucose uptake in adipocytes and skeletal muscle cells [10, 11]. All these happen within a short interval after FFA treatment, implying that the FFAs may work as signaling molecules such as hormones, to trigger signal transduction and subsequent physiological events.
During signal transduction, many intracellular signaling proteins work as molecular switches and are activated by GTP binding or phosphorylation. That FFAs acutely stimulate protein phosphorylation suggests that FFAs are able to evoke signal transduction.
When cyclooxygenase, lipoxygenase, and epoxygenase pathways were inhibited, phosphorylation was still detected, suggesting it was fatty acid, not its metabolites that triggered the phosphorylation.
In addition, increased protein tyrosine phosphorylation was also observed after treatment with oleic, linolenic and ?-linoleic acid.
In another work it was reported that unsaturated fatty acids are able to stimulate protein phosphorylation by activating protein kinase C in intact hippocampal slices [13].
Oleic acid stimulated phosphorylation of several proteins of molecular weights 92,000, 58,000, 50,000, 47,000 and 44,000 Da.
The 44,000 and 47,000 Da proteins were particularly sensitive to fatty acids and were phosphorylated in a dose- and time-dependent manner. Increased 32P incorporation into the 44,000 Da protein was apparent after 1 min and reached a maximum at 5 min. Free Fatty Acid ReceptorsDuring the last decade, a series of free fatty acid receptors (FFARs) has been identified, indicating that like other extracellular signal molecules, FFAs bind to their receptors on the plasma membrane to trigger signal transduction.
The FFARs identified belong to a large protein family, the G protein-coupled receptors (GPCRs), which are integral membrane proteins with seven trans-membrane domains. The extracellular parts of the receptors sense external signals and activate heterotrimeric G proteins to transduce signals to downstream molecules. GPCRs are activated by various types of ligands, including ions, nucleotides, amino acids, lipids, peptides, and proteins.
The known FFARs include FFAR1 (GPR40), FFAR2 (GPR43), FFAR3 (GPR41), GPR84, GPR119 and GPR120 (Table 1). GPR40 is abundantly expressed in the pancreas, and is especially enriched in pancreatic ?-cells. When activated by FFAs, GPR40 activates G-protein, which transduces the signal leading to stimulation of insulin secretion. SCFAs are generated by bacterial fermentation of undigested carbohydrates from ingested dietary fiber in the gut. Subsequently SCFAs are released in the bloodstream and accumulate to micromolar concentrations.GPR41 is expressed abundantly in adipose tissue, enteroendocrine cells, and sympathetic ganglia. SCFAs activate GPR41 and stimulate leptin expression in mouse adipocytes and mouse primary-cultured adipocytes. Overexpression of exogenous GPR41 and knockdown of GPR41 by RNAi regulates leptin production positively and negatively.
Given that leptin is a potent anorexigenic hormone that reduces food intake, propionate may inhibit food intake by increasing leptin release. The analysis of GPR41-deficient mice showed that GPR41 is expressed in enteroendocrine cells, and GPR41 deficiency is associated with reduced expression of PYY [20]. These results indicate that GPR41 activation of sympathetic neurons may involve G??, PLC?, and MAPK.GPR43 is highly expressed in immune cells, spleen, and bone marrow, and is also detected at low levels in the placenta, lung, liver, and adipose tissues [22]. A study on adipocytes showed that acetate and propionate can reduce lipolytic activity and thus plasma FFA level in a mouse in vivo model.
This inhibition of lipolysis is abolished in adipocytes isolated from GPR43 knockout animals [24]. OEA is a peripherally acting agent that reduces food intake and body weight gain in rat feeding models, suggesting that GPR119 might mediate the OEA-induced reduction of food intake [28]. Lysophosphatidyl choline (LPC) is another bioactive lipid mediator that activates GPR119 to stimulate insulin release from pancreatic islets, via Gs activation which leads to cAMP production [29].
GPR120 is highly expressed in the human and mouse intestinal tract, as well as in adipocytes, taste buds, and lungs [32, 33]. GRP120 activation by saturated FFAs with a carbon chain length of 14–18, and by unsaturated FFAs with a chain length of 16–22 has been detected [32].
Activated by medium- and long- chain fatty acids, GPR120 increases insulin secretion indirectly by stimulating the secretion of glucagon-like peptide-1 (GLP-1), the most potent insulinotropic incretin, which is coupled to the elevation of Ca2+ and activation of the ERK cascade [32]. In addition, GPR120 is also reported to function as an ?-3 FA receptor in proinflammatory macrophages and mature adipocytes that mediates the potent anti-inflammatory effects of DHA and EPA by inhibiting both the TLR and TNF- inflammatory signaling pathways [37]. Chronic tissue inflammation is another important mechanism causing insulin resistance, so the effect of GPR120 on insulin sensitivity as well as on the stimulation of insulin-secretion will make it an attractive drug target for diabetes-therapeutic agents.The discovery of FFARs developed our understanding of the role of FFAs as signal molecules.
Cells expressing FFARs, such as pancreatic ?-cells, adipocytes, and macrophages sense FFAs and make various corresponding responses to control metabolic homeostasis (Figure 2).
A few reports indicate that fatty acids have acute effects on glucose uptake, but conclusions have been inconsistent and the underlying molecular mechanisms controlling these responses are still elusive. Although both adipocytes and skeletal muscle cells are able to ingest glucose by stimulation of FFAs, skeletal muscle consumes more than 70% of the plasma glucose, suggesting that whole body plasma glucose concentration is tightly associated to the sensitivity of muscle tissue to insulin [39, 40].

We therefore focused on the molecular mechanism of fatty acid-induced glucose uptake in skeletal muscle cells [41].2.
When L6 cells were treated with palmitic acid (PA), the most abundant free fatty acid in the blood, glucose uptake increased rapidly in a time-dependent manner, beginning from 5 min, and reaching a peak at 20 min (Figure 3, lower panel).
By incubating intact PA-treated L6-GLUT4myc cells with myc antibody to detect plasma membrane-located GLUT4, we found that PA stimulates GLUT4 translocation from the cytosol to the plasma membrane (Figure 3, upper panel).
The stimulatory effects of PA on glucose uptake and GLUT4 translocation are similar to those of insulin. Fluorescence imaging shows GLUT4 translocation to the cell surface after L6-GLUT4myc (L6) cells are treated with (upper right panel) or without (upper left panel) PA or insulin (upper middle panel).
The lower panel shows that glucose uptake increases in a time-dependent manner when L6 cells are treated with PA.Akt plays an important role in insulin-stimulated GLUT4 translocation and glucose uptake.
During PA treatment, Akt phosphorylation was detected after 10 min, peaked at 45 min, then decreased dramatically after 1 h, and became nondetectable after 3 h. When treated with different concentrations of PA, Akt phosphorylation increased with PA concentration, beginning from 0.2 mM. Such time- and dose-dependent responses to PA treatment in cells match the characteristics of signal transduction, and so it is possible that a signal transduction cascade initiated by PA leads to the activation of Akt.
To further verify the stimulatory effect of PA on Akt activation, we treated rat skeletal muscle tissue with PA. AMPK is a heterotrimeric complex composed of a catalytic ? subunit and regulatory ? and ? subunits, which together make a functional enzyme that plays a role in cellular energy homeostasis [43].
Upon activation, AMPK decreases energy consumption by inhibiting fatty acid and protein synthesis and enhances energy production by stimulating fatty acid oxidation and glucose transport to increase cellular energy levels. While it is known that AMPK? is phosphorylated at Thr258 and Ser485, its upstream kinases still need further study [45]. AMPK phosphorylation (Thr172) starts as early as 5 min after PA treatment and reaches a peak at 20 min. Western blotting and glucose uptake assay results showed that all of these proteins participate in signal transduction.We applied API-2, an Akt selective inhibitor, to block Akt activity. As a result, API-2 abolished Akt phosphorylation as well as significantly decreasing PA-induced glucose uptake (Figure 7, left panel). Glucose uptake assays showed that PA-induced glucose uptake decreased when Akt expression decreased due to RNAi (Figure 7, right panel).
Together, these data suggest that PA induces glucose uptake in skeletal muscle cells via Akt activation.To study the role of AMPK in PA-induced glucose uptake, we used AMPK inhibitor Compound C, an myc-tagged AMPK dominant negative (AMPK-DN) plasmid, and siRNA targeting AMPK catalytic subunits ?1 and ?2. Since AMPK and Akt activation was observed sequentially in PA-treated cells, we also examined the relationship between AMPK and Akt. AMPK inhibitor Compound C suppressed AMPK activity and decreased PA-induced Akt phosphorylation and glucose uptake (Figure 8, left panel). Furthermore, an siRNA duplex mixture targeting AMPK ? decreases PA-stimulated Akt phosphorylation in L6 cells (Figure 8, right panel), consistent with the inhibitor and AMPK-DN experiments. In contrast, when AMPK agonist AICAR was used to stimulate AMPK phosphorylation, Akt was also stimulated rapidly in a time-dependent manner (Figure 9), suggesting that it is possible to stimulate Akt via AMPK activation in L6 cells.
When we used PI3 Kinase (PI3K) -specific inhibitor LY294002 to treat L6 cells, PA-induced glucose uptake was totally abolished (Figure 11, upper panel), suggesting that PI3K may control these two pathways.
Palmitate stimulates Akt phosphorylation via binding to the plasma membraneAs shown in Figure 12, how PA activates PI3K is still unknown. According to our current understanding of signal transduction, we speculate that PA may bind to a protein on the cell plasma membrane to trigger signal transduction.
We performed fatty acid binding assays to test this hypothesis.L6 cells were incubated with PA at low temperature (4°C) to facilitate PA binding to the cell surface while preventing its internalization, then washed with buffer to remove unbound PA, or with BSA solution to remove not only unbound but also some membrane-bound PA by competitive binding, Cells were then transferred to 37°C to recover cellular activity.
The amount of PA which binds to the cell surface was measured by adding trace amounts of 3H-labeled PA to the solution. Results showed that after washing, with either buffer or BSA solution, very little PA remained (Figure 13, upper panel). When these cells were transferred to 37°C, Western blot results showed that Akt phosphorylation took place at a similar level to that in cells kept at 37°C, and increased in a time-dependent manner in buffer-washed cells, while p-Akt was not detectable in BSA solution-washed cells (Figure 13, lower panel). These results suggest that the amount of cell surface-bound PA was sufficient to activate Akt; intracellular PA accumulation was not required. Moreover, based on lipid analysis by TLC, fatty acids were the main component of total lipids during cell treatment with fatty acid and the 10 min incubation at 37°C. Future workCould the postulated cell membrane protein which binds to FFAs and triggers signal transduction to stimulate glucose uptake in skeletal muscle cells be a G-protein coupled receptor? Therefore, a GPCR on the plasma membrane of skeletal muscle cells may be the FFA receptor we have postulated. It is thus likely that our postulated FFAR may function using long-chain FFAs as its ligands. The known long-chain FFARs include GPR40 and GPR120, both of which are related to insulin secretion.
We therefore conclude that known long-chain FFARs GPR40 and GPR120 are not our postulated FFA receptor. Our postulated receptor might therefore be a novel FFAR whose function is to stimulate glucose uptake in skeletal muscle tissue. Like GPR40 and GPR120, our postulated FFAR is also related to metabolic homeostasis, and so it is likely to be a potential drug target for the treatment of diabetes. Identification of this FFAR is one of our goals.Another significant implication of our results is that PA plays two opposing roles in skeletal muscle. Under chronic treatment it inhibits insulin-stimulated glucose uptake by blocking Akt phosphorylation, while it enhances glucose uptake by activating Akt when cells are exposed to PA for a short time.
What is the relationship between the long-term and short-term effects of FFAs on glucose uptake? We thus conclude that phosphorylation of Akt may require high concentrations of fatty acids under physiological situations. Akt phosphorylation is not detectable 3 h after fatty acid treatment (Figure 5, upper panel). In addition, when fatty acids are withdrawn, the Akt phosphorylation signal disappears after 3 h in C2C12 cells (data not shown), suggesting that fatty acid-induced phosphorylation and dephosphorylation of Akt can be completed within one cycle of a postprandial FFA wave.
It is therefore possible that Akt phosphorylation and dephosphorylation occur again and again as the concentration of FFA increases and decreases. Plasma FFA concentration starts to rise from 2 h after a meal (Figure 1) and continues to rise until the next meal due to the release of FFA from adipocytes during fasting. Based on our findings, when increasing plasma FFA reaches a certain level it stimulates Akt phosphorylation and glucose uptake. In obesity patients, elevated plasma FFA probably reaches the FFA level triggering Akt phosphorylation earlier during a plasma FFA wave, leading to abnormal glucose uptake.
Many abnormal fatty acid cycles may contribute to the development of insulin resistance by disturbing glucose homeostasis. This Yin-Yang balance of PA in skeletal muscle is likely to be physiologically significant, and the possibility of its involvement in the development of insulin resistance needs to be investigated further.4. ConclusionFree fatty acids (FFAs) function as signal molecules by activating their receptors in the cell plasma membrane to evoke signal transduction by a series of protein phosphorylation events, eventually leading to physiological events. Some of the known cell responses to FFAs are directly or indirectly related to metabolic homeostasis, so the study of FFA-triggered signal transduction will help us to understand the development of metabolic disorders and to design strategies for therapy.

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