Nutrition is a language. Poor gut balance and as what the authors call "richness" contributes to metabolic dysfunction and obesity. This study found that Nutrition can improve gut bacterial balance and "richness" that then will improve the metabolic impact of the nutrition. Complex and beautiful nutrition--gut--metabolism connection.
Gut bacteria diversity, the authors of this study called it "richness" associated with decreased inflammation and obesity. Lower gut diversity associated with increased inflammation and obesity.
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The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal
components through pattern-recognition receptors
TLRs are PRRs that recognize microbe-associated molecular patterns
TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain
homologous to the IL1 receptor intracellular domain
The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6,
which are also elevated in obese and insulin-resistant patients
Obesity,
high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
Probiotics,
prebiotics, and antibiotic treatment can reduce LPS absorption
LPS promotes hepatic insulin
resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting
the progression of fatty liver disease.
In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and
adhesion molecules, which promotes atherosclerosis development and progression.
In the adipose tissue, LPS induces adipogenesis,
insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
the gut microbiota has been recently proposed to be an environmental factor involved
in the control of body weight and energy homeostasis by modulating plasma LPS levels
dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a
bacterially related factor might be responsible for high-fat diet-induced obesity.
This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in
Bifidobacterium and Eubacterium spp.
n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able
to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a
meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component
of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of
LPS-mediated nutritional changes.
This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can
beneficially affect the host's weight and adiposity.
endotoxemia was independently
associated with energy intake but not fat intake in a multivariate analysis
in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and
decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
T2DM patients have mean values of LPS that are 76% higher than healthy controls
LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both
peripheral and hepatic
LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression
of alcoholic and nonalcoholic fatty liver disease
The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted
in bile
All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases
hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed,
with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions
such as obesity and metabolic syndrome
It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing
to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride
accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines
like TNFα
high-fat diet mice presented with ME, which
positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and
F4/80 (a specific marker of mature macrophages) mRNAs
prebiotic administration reduces intestinal permeability
to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative
stress, and macrophage infiltration markers
This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat
diet situation
high-fat feeding is associated with adipose
tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between
ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
LPS has been shown to promote atherosclerosis
markers of systemic inflammation such as circulating bacterial endotoxin
were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory
state.
small study finds diet rich in whole grains compared to refined grains improves gut bacteria balance and immune system. Maybe the key to optimal gut health is the diet?
diet and exercise increases BDNF. Diets rich in omega 3, curcumin, and polyphenols increase BDNF and thus increase neuroplasticity and associated cognition. In contrast, sugar and saturated fats in crease oxidative stress and worsened spatial learning. This study is a review.
PRP Therapy or Platelet Rich Plasma Therapy is an effective non-surgical hair loss treatment for men and women. PRP Therapy makes efficient utilization of a growth enhancing blood constituent called platelets, which when combined together with plasma, results in an unprecedented increase in the hair follicles across the treated areas.
The measurement of free cortisol in saliva provides a psychologically stress-free and reliable technique to assess the cortisol response to a standard protein-rich meal, ie, a physiological challenge to the HPA axis in men and women that could be investigated in naturalistic settings outside the laboratory.
Are you worried you are getting heavier day by day? Well, it might be because of those fries you are addicted to. Deep fried foods are rich in trans fats which are directly related to obesity and heart failure. Trans fats build up the blood vessels, hindering the smooth flow of blood through them.
The walnut benefits can also be useful for weight loss purpose. The containing omega-3 inside the walnut have fatty acids with other substances into it. The 2.5 grams of 'ALA' per serving is found rich beneficial sources as the fatty acid. From studies among the women's observed that having a walnut at diet can be helpful for reducing the weight loss with greater efficiency. It also lowers the 'bad' levels of LDL cholesterol from the body. And the higher levels of 'HDL' cholesterol in a good manner as suggested by the doctors.
increased densities of T-cell infiltrates with a high proportion of CD8+ T cells within primary colorectal carcinomas were associated with a significant protection against tumor recurrence
coexpression of genes mediating cytotoxicity and TH1 adaptive immune responses accurately predicted survival in patients with colorectal carcinoma independently of the metastatic status.
Proinflammatory cytokines secreted by inflammatory cells can contribute to tumor progression, and soluble factors produced by the tumor in response to nonspecific or tumor-specific signals, such as prostaglandin E2 (PGE2), adenosine, or TGF-β, downregulate functions of immune cells
they are largely ineffective in arresting tumor growth, although they can proliferate and mediate antitumor cytotoxicity on their removal from the tumor bed and ex vivo IL-2 activation.42
DCs (HLA-DR+CD86+CD80+CD14−) are nature’s best APCs
They are a common component of tumor immune infiltrates and are responsible for the uptake, processing, and cross-presentation of TAs to naive or memory T cells, thus playing a crucial role in the generation of tumor-specific effector T cells
DCs control the induction of Treg cells. In patients with cancer, cellular interactions between antigen-presenting DCs and T cells lead to expansion and accumulation of Treg cells at the tumor site and in the periphery
NK cells (CD3−CD56+CD16+), which mediate innate immunity and contain both perforin-rich and granzyme-rich granules, are well equipped to mediate lysis of tumor cells
B cells (CD19+, CD20+) are also rare in most human tumors, with the exception of breast cancer and melanoma
The initial acute inflammation involving the recruitment and influx of antitumor effector cells is replaced by chronic inflammation in later stages of tumor progression
Tissue hypoxia plays a major role in shaping the nature of immune infiltrates in tumors
Another great review of the immune system during different stages of carcinogenesis; how the cancer manipulates the immue system to cloak itself from the immune system.
Good review of the current data on the role of nutrition in Parkinson's disease. Take home, a lot of data is conflicting. But the figure at the end does well to summarize: diet rich in polyphenols in fruits/veggies, carotenoids, resveratrol, Vitamin C, D, E, and MUFA and PUFA are neuroprotective compared to dairy being neurodegenerative.
Purple represents #ambition, #royalty and #richness.
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https://youtu.be/eOJyG_hGa4o
Faculty: Sanjib Nath Debasmita Chattopadhyay
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Not that I am proposing gastric bypass for weight loss. IN my mind that is like a lobotomy for headache. But, this study shows the link between gut bacteria and obesity. This study documented an increase in the expression of certain bacteria types in the gut. This was associated with increase in white adipose tissue gene expression. Linking directly the gut and fat.