Insulin Can Be Irresistible.

FriendlyBugs Although it’s an understatement to say many are recommending sugar restriction as a means to improving health, evidence – relating to inflammatory conditions like insulin resistance, obesity and diabetes – indicates that this approach is unsafe, and can end up becoming a powerful driver of worsening inflammation and disease.

A good way to understand how this might be able to happen, is to look at how exposure to stress, in combination with lack of sugar availability, can inhibit metabolic function, and promote factors which can lead to increased biochemical stress. Many of these factors are central to the progression of the inflammatory blood sugar and insulin dysregulated conditions. Problems relating to digestion, tend to be more relevant than most realize.

“Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients…an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently…obesity, T2D, and CVD [cardiovascular disease] share a metabolic milieu characterized by insulin resistance and chronic subacute inflammation.”

“The present study examined the relationships between cortisol and related parameters of IR…possible pathophysiological mechanisms for the association between…stress and IR or diabetes involve hyper-stimulation of the HPA axis due to stress…chronic stress was associated with IR and may contribute to the development of IR.”

“Central to metabolic diseases is insulin resistance associated with a low-grade inflammatory status…we looked for a molecule involved early in the cascade of inflammation and identified LPS (bacterial endotoxin)…LPS is a strong stimulatory of the release of several cytokines that are key inducers of insulin resistance.”

When stress is high and sugar intake is restricted, glycogen stores are fast depleted, and the stress hormones, cortisol and adrenaline, will generally rise, as part of a process which is designed to provide alternative sources of fuel.

Adrenaline helps get the remaining glycogen out of storage and releases fat from tissue, in the form of free fatty acids. Cortisol breaks down muscle and other tissue, so that it can be used for the provision of more energy. The stress substances are crucial for survival, however when they are chronically or excessively raised, they can promote degeneration and disease.

If the fatty acids released out of storage into circulation as a result of stress, are made up of high levels of the polyunsaturated fats (PUFAs), they can have a long term negative impact upon numerous biological processes, known to be involved in the progression of insulin related problems.

PUFAs and their breakdown products, are able to promote the development of a chronic inflammatory stress state, responsible for encouraging insulin dysfunction (and many related metabolic issues), in a manner which can become self-perpetuating, and difficult to reverse. The PUFAs are highly unstable, and can easily and rapidly break down inside the human body.

“Oxidized derivatives of linoleic acid…may be involved in the increased glucocorticoid production observed in obese humans.”

“Increased MDA [Malondialdehyde, breakdown product of PUFAs]…was a risk factor for non-alcoholic steatohepatitis…insulin resistance in NAFLD correlates with enhanced oxidative stress. Histopathological disease severity significantly correlated with oxidative stress parameters…”

“…lipogenic enzyme mRNAs were markedly reduced with increasing dietary corn oil in a dose dependent fashion…PUFA-mediated suppression of the mRNA…was partially restored by pioglitazone treatment…effects…seem to be due to increased insulin sensitivity.”

“Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus…c-Jun amino-terminal kinases (JNKs) can interfere with insulin action…and are activated by inflammatory cytokines and free fatty acids, molecules…implicated in the development of type 2 diabetes.”

“…accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB.”

The greater the exposure to the stress promoting, inflammatory byproducts of the degradation of PUFAs, the more this is likely to interfere with insulin function and proper blood sugar regulation. This can then go on to cause further stress, inflammation, and overall damage to metabolism. Intestinal bacterial issues are often intertwined with these kinds of metabolic problems. Sugar is protective against stress.

The byproducts of the PUFAs, directly (and indirectly) stimulate the release of the stress substances (including cortisol, adrenalin, serotonin, nitric oxide and estrogen) and can powerfully inhibit thyroid performance, suppressing mitochondrial energy metabolism. A slow metabolism, with increasing exposure to the PUFAs, tends to impede proper digestion. Sugar increases metabolism and inhibits polyunsaturated free fatty acid release.

A sub-optimal thyroid metabolism and digestive system, allows for bacteria to feed and grow in quantity, moving further up into the small intestine where it is not preferable for them to be, promoting exposure to harmful and inflammatory bacterial toxins like endotoxin (LPS). Endotoxin causes serotonin production to be increased.

“…the gut microbiota plays a key role in promoting levels of colon and blood 5-HT (serotonin)…select microbes and their metabolic products can be used to promote endogenous, localized 5-HT biosynthesis…”

“…results further support the current view that the gut microbiota plays a crucial role in promoting the production of biologically active, free 5-HT.”

Increased circulating serotonin levels have been shown to be an important factor involved in the promotion of blood sugar dysregulation and insulin issues, which often lead to obesity and diabetes.

“Recent studies revealed that peripheral 5-HT [serotonin] plays an important role in metabolic regulation in peripheral tissues, where it suppresses adaptive thermogenesis in brown adipose tissue…suppressing 5-HT signaling might represent a new target for anti-obesity treatment by increasing energy expenditure and improving insulin resistance.”

“SERT-deficient mice exhibit hyperglycemia and insulin resistance, both of which are characteristic features of diabetes.”

Serotonin and endotoxin have both been demonstrated to promote inflammation, and to inhibit mitochondrial energy metabolism, leading to further stress and circulation of PUFAs, interfering with the proper use of sugar. Examining ways to improve digestion, in order to minimize bacterial issues, makes a lot of sense in the context of inflammatory conditions which rise under stress, and are associated with insulin resistance.

“Latest evidence suggests…bacterial LPS (endotoxin) deriving from the gut microbiota may trigger inflammation and oxidative stress in response to diets…This “metabolic endotoxemia” has been shown to initiate or promote obesity, insulin resistance, metabolic syndrome, and finally diabetes.”

“A striking inflammatory response is septic shock. We tested the hypothesis that non-neuronal serotonin enhances this neutrophil-driven disorder…Indeed, Tph1-/- mice were protected from lethal LPS-induced septic shock…The release of serotonin is yet another way by which platelets enhance inflammatory responses. Excessive neutrophil recruitment may thus also become a target of antiserotonergic treatment strategies.”

Contrary to popular beliefs, there is good evidence showing that rising serotonin is an important element involved in the progression of depression. Endotoxin and inflammation are also closely connected to depression, and depression and diabetes often go hand in hand.

“…endotoxaemia and inflammation owing to increased intestinal 5-HT may underpin the depression and diabetes association, where the risk of the latter pathology becomes particularly preeminent after the onset of depression…”

Stress and lack of sugar, combined with a lot of exposure to PUFAs, powerfully suppresses thyroid energy metabolism and digestive function, also impacting upon intestinal barrier capabilities. Interference with the gut barrier, is potentially far more dangerous when bacterial issues exist, as more of the toxic bacterial byproducts, like endotoxin, have the opportunity to pass through to the liver. Serotonin excess has also been shown to promote intestinal permeability.

If the liver becomes stressed and overloaded, this can interfere with detoxification functions, which means that potentially harmful substances produced in the intestine (such as bacterial endotoxin and serotonin) are able to pass into the main system in greater quantities, where they promote further inflammation, aggravating problems associated with insulin function and diabetes. The combination of the PUFAs, high serotonin and endotoxin, is inflammatory and anti-metabolic, and apart from their diabetogenic effects, these things can be involved in the progression of nonalcoholic fatty liver disease (NAFLD), obesity and heart disease.

“…high-fat feeding dramatically increased intestinal permeability…gut bacteria are involved in the control of intestinal permeability and furthermore in the occurrence of metabolic endotoxemia.”

“Compelling evidence supports the concepts that gut microbiota actively promotes weight gain and fat accumulation and sustains, indirectly, a condition of low-grade inflammation, thus enhancing the cardiovascular risk.”

“Previous studies suggested that alterations in intestinal motility and permeability contribute to the development of NAFLD…treatment…caused a reduction of elevated serotonin levels… resulting in a reduction of endotoxin influx into the liver and subsequently of liver inflammation and fat accumulation.”

The liver is responsible for detoxification of estrogen for excretion. Excess estrogen interferes with liver function, inhibits thyroid performance and promotes serotonin levels, and these conditions can provoke stress and rising cortisol levels, and can encourage a general state of metabolic suppression and blood sugar dysregulation.

When stress and inflammation is high, estrogen is more likely to get trapped inside tissue, and so actual levels of estrogen in the body, are not necessarily accurately reflected in blood test results, leading to misleading (although popular) ideas with regards to ‘estrogen deficiency’, being a real circumstance involved in disease promotion. Prolactin (a substance which is connected to stress and inflammation), promotes cortisol release and is associated with insulin resistance, and prolactin levels are also known to be an accurate measure of tissue estrogen status.

As estrogen levels increase, and liver function is increasingly interfered with, thyroid hormone can be less able to be converted into the metabolically active form (T3), further adding to stress and the suppression of energy system function, leading to greater release of the polyunsaturated free fatty acids, and worsening inflammation and insulin resistance.

Rising levels of endotoxin, serotonin and estrogen in combination with high levels of exposure to the PUFAs, seem to go together with rising stress, causing a worsening of inflammation and insulin resistance, and exacerbation of bacterial issues, generally increasing the likelihood of obesity, diabetes, and cardiovascular disease, and other inflammatory conditions.

“…evidence suggests that changes in intestinal microbial composition could be responsible for increased endotoxemia in response to a high-fat diet, which in turn would trigger the development of obesity and diabetes.”

“Experiments…have shown that endotoxin is associated with cardiometabolic abnormalities including obesity, insulin resistance, and diabetes….Importantly, a high-fat diet increased the proportion of…LPS-containing microbiota in the gut.”

“In vivo experiments have demonstrated that injections of bacterial endotoxins induce systemic inflammation, which is accompanied by the appearance of insulin resistance…serum LPS [endotoxin] activity is inversely correlated with insulin sensitivity both in diabetic and nondiabetic cohorts.”

Bacterial endotoxin is directly inflammatory, and both endotoxin and inflammation can promote levels of the stress substance nitric oxide, which suppresses thyroid energy metabolism, and is another factor in the development of insulin resistance and related metabolic issues.

“Increased nitric oxide (NO) production, especially as a consequence of inducible nitric oxide synthase (iNOS), has also been implicated in insulin resistance, especially in the context of obesity…iNOS is markedly increased in macrophages and other inflammatory cells stimulated by proinflammatory cytokines.”

“LPS [endotoxin] and the accompanying inflammatory stress markedly impair insulin stimulated muscle glucose uptake as well as induce cardiovascular dysfunction…an increase in NO availability alone in the absence of an inflammatory stress markedly impaired insulin-stimulated MGU [muscle glucose uptake]…”

“Considering the hyperactivity of the inducible NO synthase in MS [metabolic syndrome], these data confirm the altered redox and inflammatory status that characterizes the MS and suggest a link between lipid peroxidation, inflammation, and insulin resistance…examination…shows… in particular, a significant positive association between NOx and the degree of insulin resistance.”

Stress and the suppression of oxidative metabolism, means that lactate levels go up, worsening insulin resistance and increasing diabetes risk. Lactate has also been shown to be a driver of cancer, and evidence suggests that high lactate is one of the reasons for the link between cancer and diabetes. Low blood sugar promotes lactate.

“Accumulative evidence indicates a high incidence and mortality for a variety of malignancies in patients with diabetes…Diabetes and cancer interact with each other in a vicious cycle, where lactate plays a pivotal role in this mutual interaction. Insulin resistance/diabetes and cancer conditions produce high levels of lactate and conversely high lactate promotes diabetes and cancer development and progression…”

Depending on individual metabolic circumstances, sugar restriction (especially when it is attempted in order to help with already existing problems), can be just the thing needed to set in motion a cascade of interrelated, often synergistic, stressful and inflammatory changes, which are popularly, although inappropriately blamed on the consumption of too much sugar.

Lack of sugar increases cortisol and free fatty acids, which can inhibit thyroid function and digestion, promoting bacterial endotoxin. Endotoxin increases inflammation, and can cause estrogen, serotonin and nitric oxide to rise, stressing the liver. Low sugar also reduces liver function, allowing for systemic inflammatory issues to rise. Endotoxin, nitric oxide, serotonin and estrogen suppress oxidative metabolism, increasing lactate, and these things can promote each other, and further fuel the inflammatory response, increasing stress and insulin resistance, potentially turning into a self-feeding downward spiral. Stress and high cortisol from sugar restriction magnifies the inflammatory response to endotoxin.

“…transient elevation of in vivo cortisol concentrations to levels that are observed during major systemic stress enhanced a subsequent, delayed in vivo inflammatory response to endotoxin. This appeared to be a dose-dependent effect that was more prominent at intermediate concentrations of cortisol than at higher concentrations of cortisol.”

Carbohydrate consumption (in particular the difficult to digest starchy, fibrous foods) can under some circumstances, promote bacterial overgrowth and endotoxemia, although this is far more likely to be true when it is consumed in combination with PUFAs, when stress is high and when metabolism and digestion are already less than optimal. Although I’m not a doctor or nutritionist, and this is not medical or health advice, my experience has shown me that at times like this, it is even more important to experiment with ways to ensure that sugar and protein and other nutrients can be supplied in a manner which is as easy as possible for digestion. High fat, high carb meals, especially those which are high in PUFAs and starches, can be inflammatory and can add to bacterial, insulin and blood sugar issues.

“HFHC (high PUFA high carb) meal…induces an increase in plasma LPS (endotoxin)…relevant to the pathogenesis of postprandial oxidative and inflammatory stress, insulin resistance, and atherosclerosis…”

Orange juice – as well as white sugar or sugar from fruit in general – can protect against stress, lowering exposure to endotoxin, estrogen, serotonin, nitric oxide, lactate and cortisol. From this perspective, sugar can be seen as an anti-inflammatory, anti-diabetes, pro-metabolism food.

“The combination of glucose…and the HFHC meal induced oxidative and inflammatory stress and an increase in…endotoxin….orange juice intake with the HFHC meal prevented meal-induced oxidative and inflammatory stress…”

Even though it is true that the consumption of any kind of fat can cause a temporarily insulin resistant state, it is the PUFAs which are known to stimulate a chronic rise in inflammation, and which help prevent the return to normal function, when stress is lowered and sugar for fuel is available. One of the benefits of the highly saturated fats, like coconut oil for instance, is that they are anti-inflammatory, and have anti-bacterial properties.

“Our findings provide evidence for early biological adaptations to high fat feeding that proceed and possibly lead to insulin resistance…our study is the first to demonstrate that circulating endotoxin concentrations are increased following 5 days of an isocaloric, HFD [30% carbohydrate, 15% protein, and 55% fat (25% SFA)] in healthy humans.”

One of the possible benefits of a low fat (and very low PUFA), moderate protein and high carb diet, is that any excess sugar consumed will either be stored as glycogen for later use, or converted into predominantly saturated fats, which are anti-inflammatory, can be used as fuel during times of stress, and have been demonstrated not to cause long term harm to metabolic function.

A diet avoiding the PUFAs and with enough protein from milk, cheese and gelatin, with plenty of sugar from easily digestible sweet ripe fruits, fruit juice, white sugar and honey, is one way to potentially help protect against stress, promote thyroid function and energy metabolism, and help limit the blood sugar dysregulating, insulin interfering, inflammatory effects of excess exposure to endotoxin.

“Resistance to endotoxin in essential fatty acid-deficient (EFAD) rats is associated with reduced synthesis of certain arachidonic acid metabolites…Endotoxin caused a less severe change in permeability index in…EFAD (essential fatty acid deficient) rats than in normal rats…”

When enough sugar is continuously provided (in the context of a nutrient dense, easy to digest diet) and stress is able to be lowered, exposure to the polyunsaturated free fatty acids still in storage, can be safely lowered, promoting a reduction in exposure to the stress substances (including cortisol, serotonin, nitric oxide, estrogen and lactate) and together, this can allow for a gradual lowering of inflammatory issues, and an improvement in blood sugar regulation and overall metabolic performance.

The ease of digestion of a pro-metabolic high sugar, low PUFA diet, reduces stress, inhibits bacterial issues, improves gut barrier function, lowers endotoxin circulation, improves insulin sensitivity, and can protect against obesity, diabetes, heart disease, cancer and metabolic disease in general. In this sense sugar is powerfully anti-bacterial, and not the villain it is made out to be.

“…gut bacteria are involved in…metabolic endotoxemia…inflammation, and metabolic disorders. This effect could be mediated by a mechanism that could increase gut permeability and enhance LPS absorption. Antibiotic treatment significantly lowers plasma LPS levels, gut permeability, and the occurrence of…inflammation, oxidative stress…and metabolic disorders.”

Some other things which are pro-metabolism and have the potential to protect against bacterial issues and improve insulin function include magnesium, biotin, coffee and caffeine, activated charcoal, coconut oil, niacinamide, thyroid hormone, aspirin, glycine, cascara, taurine, minocycline and some other antibiotics, certain antihistamines like cyproheptadine, and pregnenolone.

The antibiotic anti-microbial effects of a daily raw carrot salad and some occasional well cooked mushrooms can also help protect against bacterial overgrowth and related insulin dysregulating effects.

See more here

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Endotoxaemia resulting from decreased serotonin tranporter (5-HTT) function: a reciprocal risk factor for depression and insulin resistance?

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Endotoxin Mediated-iNOS Induction Causes Insulin Resistance via ONOO− Induced Tyrosine Nitration of IRS-1 in Skeletal Muscle

A central role for JNK in obesity and insulin resistance.

Lactate induces insulin resistance in skeletal muscle by suppressing glycolysis and impairing insulin signaling.

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Attenuation of Lipopolysaccharide Induced Inflammatory Response and Phospholipids Metabolism at the Feto-Maternal Interface by N-Acetyl-Cysteine

Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability.

Prolactin triggers pro-inflammatory immune responses in peripheral immune cells.

Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB.

Plasma Lactate Levels Increase during Hyperinsulinemic Euglycemic Clamp and Oral Glucose Tolerance Test

Nicotinamide improves glucose metabolism and affects the hepatic NAD-sirtuin pathway in a rodent model of obesity and type 2 diabetes.

Reduced Serotonin Reuptake Transporter (SERT) Function Causes Insulin Resistance and Hepatic Steatosis Independent of Food Intake

Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine

Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E

Skeletal Muscle Lipid Peroxidation and Insulin Resistance in Humans

Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression.

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Pretreatment with stress cortisol enhances the human systemic inflammatory response to bacterial endotoxin

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Association of Oxidative Stress, Insulin Resistance, and Diabetes Risk Phenotypes

Early Skeletal Muscle Adaptations to Short-Term High-Fat Diet in Humans Prior to Changes in Insulin Sensitivity

Effect of Lipopolysaccharide on Inflammation and Insulin Action in Human Muscle

Estradiol Binds to Insulin and Insulin Receptor Decreasing Insulin Binding in vitro

Lactate, a Neglected Factor for Diabetes and Cancer Interaction

Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial.

Platelet serotonin promotes the recruitment of neutrophils to sites of acute inflammation in mice

Polyunsaturated fatty acids decrease the apparent affinity of vitamin D metabolites for human vitamin D-binding protein.

Gut Microbiota and Metabolic Endotoxemia in Young Obese Mexican Subjects

Association between insulin resistance and estrogen in sexual precocity of obese children

Activation of central lactate metabolism lowers glucose production in uncontrolled diabetes and diet-induced insulin resistance.

Chronic peripheral administration of serotonin inhibits thyroid function in the rat

Transient receptor potential M3 channels are ionotropic steroid receptors in pancreatic β cells

Bacterial Endotoxin Activity in Human Serum Is Associated With Dyslipidemia, Insulin Resistance, Obesity, and Chronic Inflammation

Serotonin as a New Therapeutic Target for Diabetes Mellitus and Obesity

The Effects of Serotonin in Immune Cells

Is hyperprolactinemia associated with insulin resistance in non-obese patients with polycystic ovary syndrome?

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Thyroid Function in Human Obesity: Underlying Mechanisms

Resistance of essential fatty acid-deficient rats to endotoxic shock.

The influence of endotoxemia on the molecular mechanisms of insulin resistance.

Obesity, Insulin Resistance and Free Fatty Acids

A role for iNOS in fasting hyperglycemia and impaired insulin signaling in the liver of obese diabetic mice.

Polyunsaturated fatty acid-mediated suppression of insulin-dependent gene expression of lipogenic enzymes in rat liver.

Oxidative stress is closely associated with insulin resistance in genotypes 1 and 3 chronic hepatitis C

Metabolic endotoxemia and diabetes mellitus: A systematic review.

Prevention of fat-induced insulin resistance by salicylate

Free Fatty Acids Produce Insulin Resistance and Activate the Proinflammatory Nuclear Factor-κB Pathway in Rat Liver

Executive functioning and diabetes: The role of anxious arousal and inflammation.

Antidepressants induce cellular insulin resistance by activation of IRS-1 kinases.

Investigation of the Relationship Between Chronic Stress and Insulin Resistance in a Chinese Population

Aging and Insulin Resistance: Just Say iNOS

Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease.

Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes

Direct effects of prolactin on corticosterone release by zona fasciculata-reticularis cells from male rats.

11β-HSD1 inhibition ameliorates metabolic syndrome and prevents progression of atherosclerosis in mice

iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents

Regulation of gut luminal serotonin by commensal microbiota in mice

Activation of Pregnane X Receptor by Pregnenolone 16 α-carbonitrile Prevents High-Fat Diet-Induced Obesity in AKR/J Mice

Oral taurine but not N-acetylcysteine ameliorates NEFA-induced impairment in insulin sensitivity and beta cell function in obese and overweight, non-diabetic men.

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Neuroendocrine perturbations as a cause of insulin resistance.

An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells.

Partial Inhibition of Adipose Tissue Lipolysis Improves Glucose Metabolism and Insulin Sensitivity Without Alteration of Fat Mass

Blocking iNOS and endoplasmic reticulum stress synergistically improves insulin resistance in mice

Chronic caffeine intake decreases circulating catecholamines and prevents diet-induced insulin resistance and hypertension in rats.

High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes.

Minocycline Attenuates Severe Hyperglycemia in Patient with Lipodystrophy

Association between serum prolactin levels and insulin resistance in non-diabetic men

Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis

Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse.

Changes in blood glucose and insulin responses to intravenous glucose tolerance tests and blood biochemical values in adult female Japanese black bears (Ursus thibetanus japonicus).

Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice.

The Effect of Estrogen Use on Levels of Glucose and Insulin and the Risk of Type 2 Diabetes in American Indian Postmenopausal Women

Macrophages Inhibit Insulin Signalling in Adipocytes: Role of Inducible Nitric Oxide Synthase and Nitric Oxide

How does brain insulin resistance develop in Alzheimer’s disease?

A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle.

Mammalian hibernation: a naturally reversible model for insulin resistance in man?

Adipose tissue function in the insulin-resistance syndrome.

Inflammation and insulin resistance

Mechanism of free fatty acid-induced insulin resistance in humans.

Effects of Aromatase Inhibition and Androgen Activity on Serotonin and Behavior in Male Macaques

Alterations of the volatile metabolome in mouse models of Alzheimer’s disease

Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences.

#sugarsaves
#thatpufafilm
#carbconfusion
#raypeat

Image: FoodsMatter: “Probiotics – the ‘friendly’ bacteria:” John Scott

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