Sugar Helps Medicine Go Down

Suga Talking about the effects of a High Fat/High Carb meal (HFHC) on metabolic function, without considering the type of fat and type of carbohydrate involved, is about as meaningful as talking about the color of cheese on Mars…it’s a reddish brown by the way.

Even though there’s probably no such thing as a perfectly controlled scientific experiment, examining the impact of diet upon metabolic health, without distinguishing between the saturated and unsaturated fats – looking at what happens when they’re ingested alone or with different amounts of glucose, fructose or sucrose – is likely to produce misleading and potentially invalid conclusions.

In fact, regular intake of starch or glucose in combination with the highly unsaturated fats can be a recipe for disaster, and lots of evidence suggests that when it comes to the creation of inflammatory and stressful disease promoting biological conditions, few things are as effective as the polyunsaturated fats (PUFAs).

“A majority of the studies on linoleic acid and its derivatives show a direct/indirect link with inflammation and metabolic diseases.”

“Adults with a diet rich in omega-6 polyunsaturated fatty acids (PUFAs) display increased stress reactivity…a maternal diet rich in omega-6 PUFAs during gestation and lactation produce changes in sociability consistent with those observed in ASD [autism].”

“Compounds…derived from linoleic acid, may affect adrenal steroid production in humans and mediate some of the deleterious effects of obesity and oxidative stress…”

“…a moderately high fat diet of coconut oil, either in the presence or absence of fructose, does not induce significant diabetic symptoms (elevated fasting blood glucose and glucose intolerance) while isocaloric diets with soybean oil (either with or without fructose) do.”

“Dietary LC n-3 PUFA are highly vulnerable to oxidation…4-Hydroxy-2-hexenal (4-HHE) and 4-hydroxy-2-nonenal (4-HNE) are major end-products derived from n-3 and n-6 PUFA peroxidation…high-fat diets containing realistically oxidized n-3 PUFA induced the highest amounts of 4-HHE and inflammatory markers in plasma.”

Consuming ‘too much’ easily digestible starch or pure glucose, can be stressful and inflammatory in its own right. Although the response to starch depends to some degree upon individual digestive and metabolic function (and upon the source of starch), the more rapid conversion of some starches into glucose in the blood, can powerfully stimulate insulin, and increase fat storage. Indigestible starches can be problematic for other reasons which I’ll discuss a little, further on.

“Glycaemia was significantly lower after the meal containing the highest amount of sugar…compared with the non-sweetened cereal…There was a significant inverse correlation between the amount of sucrose incorporated and the degree of glycaemia…plasma insulin response was significantly lower after the highest sugar meal…compared with the meal without sugar…We found a significant reduction in glycaemic and insulin responses when sugar replaced the rapidly digested starch in a processed breakfast cereal, i.e. the opposite of what is commonly believed.”

“Glucose ingestion…in healthy human subjects resulted in…an immediate increase in intranuclear NF-kappaB binding…an increase in IKKalpha, IKKbeta, IKK activity, and messenger RNA expression of TNF-alpha…consistent with profound acute pro-inflammatory changes…”

“Animals fed a low-fat, high-sucrose…diet were actually leaner than animals fed a high-complex-carbohydrate diet.”

Eating starch increases glycogen stores in the liver, but often less effectively than sucrose or fructose. The potential rapid rise in blood sugar and surge in insulin from the consumption of pure glucose or starch, can be followed by a fall in blood sugar levels, causing cortisol to increase. The addition of some fructose or sucrose can protect against metabolic stress.

“…small amounts of fructose can markedly reduce hyperglycemia during…glucose infusion by increasing NHGU [net hepatic glucose uptake] even when insulin secretion is compromised.”

“Single…doses of fructose infused have shown a ∼30% reduction in postprandial hepatic glucose output under hyperglycemic conditions in people with type 2 diabetes and a…threefold increase in glycogen synthesis under euglycemic hyperinsulinemic conditions in people without diabetes…fructose replacement of other carbohydrates resulted in clinically significant improvements in glycemic control…”

“…fructose improves the glycemic response to an oral glucose load in normal adults without significantly enhancing the insulin…response.”

The stress inducing, catabolic effects of low blood sugar and high cortisol can impact upon metabolic conditions in a variety of different ways, interfering with thyroid function, promoting the harmful effects of the stress substances (like serotonin and endotoxin), driving numerous inflammatory factors.

These kinds of stressful, inflammatory conditions, interfere with the use of sugar for energy production and can promote the progression of illness, including obesity.

“Chronic excessive glucocorticoid exposure results in whole-body insulin resistance and the development of abdominal adiposity in humans.”

“…mechanisms of posthypoglycemic insulin resistance induced by lipolysis include increase in endogenous glucose production, suppression of peripheral utilization and oxidation of glucose, and increase lipid oxidation…”

“…following regular exercise and CR [caloric restriction] there are GC[glucocorticoid]-induced mechanisms that promote adipose tissue mass gain and impaired metabolic control in healthy organisms…”

“…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.”

When a thyroid suppressed person with slow digestion, consumes under cooked or hard to digest starch, it can in many cases more easily become food for bacteria, irritating the intestines and encouraging higher levels of endotoxin and other inflammatory things to pass into the liver, and through to the main system, spreading inflammation.

A high fat meal in general can promote systemic endotoxin circulation, but starch or glucose combined with the polyunsaturated fats (PUFAs), has been shown to escalate the severity of inflammatory reactions and worsen the conditions of stress and metabolic interference in a variety of ways. Combining the starches with the highly saturated fats, appears to make them safer.

“Baseline endotoxin concentrations…increased significantly by approximately 50% after a high-fat meal or after a high-fat meal with cigarettes but not after no meal or cigarettes alone…a high-fat meal…also significantly reduced plasma endotoxin neutralization capacity, which is an indirect measure of endotoxin exposure…Low-grade endotoxemia may contribute to the postprandial inflammatory state…”

“Feeding an EFAD [essential fatty acid-deficient] diet reduces baseline inflammation and inflammatory response to endotoxin long before the development of EFAD, and added AA + DHA modifies this response…In response to lipopolysaccharide [endotoxin], the levels of tumor necrosis factor and interleukin-6 were significantly lower with HCO [coconut oil], reflecting reduced inflammation.”

“…we observed a statistically significant increase in plasma levels of LPS [endotoxin]…after the intake of the CHO-PUFA meal, whereas no postprandial changes were observed after the ingestion of the Med and SFA-rich meals.”

The PUFAs and their breakdown products are associated with blood sugar regulation issues. Evidence shows that they reduce the ability of cells to properly use glucose, and they also cause an increase in cortisol secretion. They promote the stress substances like serotonin and estrogen, and they’re responsible for rising levels of toxic free radicals, cytokines, prostaglandins and other pro-inflammatory things. They have been associated with the development and progression of many kinds of inflammatory diseases, including diabetes and cancer.

“Oxidized derivatives of linoleic acid have the potential to alter steroidogenesis…One such derivative…stimulates corticosterone biosynthesis and amplifies the effect of ACTH…Increased levels of fatty acid metabolites may be involved in the increased glucocorticoid production observed in obese humans.”

“Chronic hyperglycemia…correlated with [malondialdehyde] MDA levels, suggesting the involvement of lipid peroxidation in the pathogenesis of diabetes complications.”

“…results provide evidence that LA [linoleic acid]…can trigger activation…and expression of inflammatory mediators…highly expressed during the pathology of atherosclerosis…as well as participating in inflammatory processes…”

“Linoleic acid is a direct precursor of the bioactive oxidized linoleic acid metabolites. It is also a precursor of arachidonic acid, which produces pro-inflammatory eicosanoids and endocannabinoids…A majority of the studies on linoleic acid and its derivatives show a direct/indirect link with inflammation and metabolic diseases.”

“…we find that neutrophil-derived leukotrienes [PUFA breakdown product] aid the colonization of distant tissues by selectively expanding the sub-pool of cancer cells that retain high tumorigenic potential…”

“…corn oil rapidly activates NF-κB in Kupffer cells via oxidant-dependent mechanisms. This triggers production of low levels of TNFα which is mitogenic in liver and promotes growth of hepatocytes…sustained stimulation of cell proliferation is most likely a key step in the ultimate development of cancer in liver…”

PUFAs damage thyroid function and digestion, increasing the potentially harmful impact of starch (or sugar in general) upon metabolic function and proper blood sugar regulation, worsening the severity of bacterial endotoxin and other inflammation issues.

“Several fatty acids had potent T4 to T3 [active thyroid hormone] conversion-inhibiting activity…Significant inhibition was evident with…arachidonic acid and linolenic acid…Saturated fatty acids, such as palmitic, stearic…acids, had little or no…inhibiting activity.”

“…the production of pro-inflammatory cytokines and chemokines, and the induction of oxidative reactions by activated leukocytes and epithelial cells represent the main event in the intestinal inflammation…Polyunsaturated fatty acids…are…principal targets of oxidative modifications. These lipids…readily undergo non-enzymatic oxidation to form chemically-reactive species that can induce a wide range of biological effects including inflammation…

“…diabetes associated with dyslipidemia, even in well-controlled patients, was associated with increased lipid peroxidation. Furthermore, dyslipidemia and increased lipid peroxidation were strongly correlated with higher levels of systemic inflammation.”

This metabolic dysfunction can result in a vicious circle of stress and inflammation, which can continue to be fueled by the release of PUFAs stored in tissue, for a reasonably long time, even in the absence of excessive fat consumption.

“Cell enrichment with PUFA initiated a rise in…lipid peroxidation products…results indicate that the accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress…”

PUFAs disturb many cellular functions, but they have been shown to be able to directly interfere with metabolic energy production, damaging the oxidizing ability of the cell. Suppression of energy production, can then further increase oxidative stress. I’m unaware of evidence showing that sugar consumption itself is responsible for this kind of effect.

“…ratios of lactate dehydrogenase to citrate synthase and beta-hydroxyacyl coenzyme-A dehydrogenase to citrate synthase were increased, indicating myocardial reduction of tricarboxylic acid cycle…PUFAs increased oxidative stress in the heart by providing cardiac susceptibility to lipoperoxidation and shifting the metabolic pathway for energy production.”

“…results indicate that…PUFA-rich soybean oil is more obesogenic and diabetogenic than coconut oil which consists of primarily saturated fat. They also show that fructose is less obesogenic than soybean oil and reveal a striking fatty liver morphology induced by soybean oil…”

“…oxidative stress produced…progressive ATP depletion…Besides demonstrating a close relationship between lipid peroxidation and haemolysis, these data…strongly indicate…a profound modification of erythrocyte energy metabolism during oxidative stress.”

Sugar can be very therapeutic. Both fructose and sucrose stimulate metabolic performance, and help to limit stress induced thyroid energy system suppression, which can protect against some of the inflammatory effects of starches and the polyunsaturated fats.

“Subjects in the 3 groups ingested a 300-kcal drink of 75 g glucose…orange juice…or water along with a 900-kcal HFHC meal (egg-muffin and sausage-muffin sandwiches and 2 hash-brown potatoes that contained 81 g carbohydrates, 51 g fat, and 32 g protein)…the intake of glucose and a HFHC meal are profoundly and rapidly proinflammatory…at the cellular and molecular level…”

“Fructose virtually abolished the fasting induced…fall in glucose and insulin and rise in glucagon…fall in triiodothyronine…ketosis and acidosis…increased ammonia excretion…hyperuricemia (and hypouricosuria), and…fall in plasma alanine and rise in branched chain amino acids. Fructose also significantly reduced urinary sodium loss…fructose exerted a prominent protein-sparing action…low-dose fructose infusion essentially abolishes the entire hormone-substrate response to fasting, and spares body protein without raising insulin…”

By helping to stabilize blood sugar and improve overall metabolic function, fructose can enable the cell to burn glucose more effectively, possibly increasing the amount of starch which can be safely consumed, protecting from some of its potentially inflammatory, stress promoting, blood sugar dysregulating effects.

The saturated fats are also known to be able to protect against some of the damaging effects of the PUFAs, and reduce stress and inflammation.

“…we found that a variety of saturated fatty acids significantly suppressed an increase in ACTH release induced by CRH stimulation…In contrast…unsaturated fatty acids, oleate, linolate and arachidonate effectively enhanced ACTH release”

Ongoing exposure to stress – encouraging hypoglycemia and high cortisol – is a common cause of metabolic energy system suppression and the inflammatory blood sugar dysregulated conditions which have been shown to promote obesity and disease.

“…depression and stress elevate cortisol production…insulin secretion rises as cortisol increases…Persistent hypercortisolemia and higher insulin enhance visceral fat accumulation…Greater numbers of prior day stressors were also associated with lower fat oxidation as well as higher insulin production. People with lower fat oxidation are more likely to gain weight by storing fat than those with higher fat oxidation, and thus their risk for obesity is increased. Higher levels of insulin are lipogenic, further enhancing fat storage.”

Fructose and sucrose effectively promote glycogen storage, and improved glycogen availability can help protect against stress and improve metabolism, reducing inflammation from free fatty acid release and excessive endotoxin exposure.

“…drinks with added fructose or galactose…were twice as effective as…glucose in restoring liver glycogen…”

“…ingested in the form of glucose–fructose mixtures (or sucrose), not only is this ingestion rate more tolerable due to lower gut discomfort but total body glycogen status can also be enhanced over glucose…alone, due to greater liver glycogen repletion.”

Incessant exposure to a variety of stress promoting factors can combine to have a major impact upon metabolism. Rather than demonizing nutritious foods (lumping together many things that differ greatly in effect), it makes more sense, for starters, to explore some of the finer details regarding how the composition of fats and sugars can either promote, or help reduce biological stress.

I’m not saying don’t eat starch if you like to eat starch, nor am I saying you must eat lots of sugar and have no fat in your diet. In fact, I’m not saying what to do or what not to do at all. I’m not a doctor or a scientist, and I eat lots of potatoes. This is just ideas and information to consider, and there is plenty of information in the studies included. Do with it what you will.

The relationship between stress and sugar is well documented, as is the relationship between the PUFAs and inflammatory metabolic illness. A consistently low supply of sugar can often mean that cortisol stays high, and that there will be a greater level of exposure to polyunsaturated free fatty acids and other promoters of inflammation and metabolic suppression. This can create a situation where an inflammatory stress state becomes chronic, sometimes with a virtual inability to revert back to proper metabolic function.

“Glucocorticoids…are critical in the regulation of energy homeostasis, and liberate energy substrates for mitochondrial oxidation during stress by enhancing muscle protein breakdown, adipose tissue lipolysis, hepatic gluconeogenesis, and reducing glucose utilization, all of which elevate circulating glucose concentrations…Chronic excessive glucocorticoid exposure results in whole-body insulin resistance and the development of abdominal adiposity in humans.”

Consumption of sugar can sometimes be enough to switch off the stress response, significantly limit fatty acid exposure, and create the conditions required for improved mitochondrial energy production.

“…carbohydrate restriction may be the predominant factor responsible for the decreases in resting metabolic rate observed with the hypocaloric diets…sucrose replacement increase the resting metabolic rate by 200 to 250 kilocalories per day…sufficient to accelerate the loss of body fat by nearly 1kg per month.”

Sugar (and improved thyroid performance) can help divert away from the inflammation and the stress promoting substances, including endotoxin, serotonin, estrogen, nitric oxide, lactate and histamine. Orange juice has many beneficial and protective ingredients, including sugar.

“Caloric intake in the form of orange juice or fructose does not induce either oxidative or inflammatory stress…”

“…the intake of orange juice was able to neutralize the oxidative and inflammatory stress caused by the HFHC meal and the associated increases in…endotoxin concentrations…”

Improved glycogen storage and supply helps to lower cortisol, and protects against the inflammatory by-products of the excessive breakdown of muscle tissue, which often results from stress, low blood sugar and exposure to PUFAs.

It is potentially very misleading to refer to the inflammatory effects of high sugar or fatty foods, when the actual ingredients of these foods can vary so greatly. The real issues are metabolic suppression, blood sugar dysregulation, inflammation and stress. Some kinds of ‘sugar’ and ‘fat’ are better than other kinds at causing or encouraging these issues. Some kinds, are better at protecting against, and reversing them.

Scientific experiments often fall short of providing useful information, capable of improving clarity of understanding. Instead, by grouping things inappropriately, and misrepresenting the significance of findings, they can end up adding to the confusion.

Foods listed as being high in saturated fats are very often made up of high levels of MUFAs and PUFAs, which are not accounted for when discussing outcomes. Extreme quantities of the different kinds of carbohydrates are sometimes used to cause unrealistically harmful results. High fat or carb, versus low fat or carb meal percentage differences are often insignificant. Other potentially metabolism interfering ingredients in meals being used for studies, are commonly ignored. Short term symptom reduction due to stress can be treated as though it is representative of long term beneficial effects, when the opposite can be true. The combined effects of inflammatory and protective foods, potentially draw attention away from the dangers of the problematic ingredients.

“…there may be food products that may be noninflammatory and protective against the proinflammatory effects of other foods. These observations are relevant to the role of postprandial inflammation in the pathogenesis of atherosclerosis, cardiovascular disease, and insulin resistance.”

When the intention is genuinely to discover the truth and promote awareness, there are many effective ways to approach an experiment, which can be enlightening, however, many studies appear as though they are working towards predetermined objectives.

Comparing a group being fed a high sucrose or fructose/saturated fat meal, with a second group being fed a high PUFA/starch meal, and other groups being fed fat free/sucrose or glucose meals is one possible way. There are many ways to tweak studies in order to get more informative and useful results.

The fact that orange juice can have an anti-inflammatory effect when consumed with very inflammatory foods is important to know. Knowing what is making the foods inflammatory in the first place is equally, if not more important. It is interesting that this part of the story is often ignored.

“…the intake of orange juice in combination with an HFHC meal prevents…the inflammatory response…”

If the study results were to show that a saturated fat, high sucrose meal is protective in its own right, surely that would make the potential conclusions more meaningful and useful.

“…dietary MCFAs/MCTs [coconut oil] suppress fat deposition through enhanced thermogenesis and fat oxidation in animal and human subjects…several reports suggest that MCFAs/MCTs offer the therapeutic advantage of preserving insulin sensitivity in animal models and patients with type 2 diabetes.”

“If a massive amount of glucose is consumed in the brain during stress, therefore, it is possible that feeding a high-sucrose diet contributes to counteracting stress.”

“…we observed a 21 percent reduction in resting metabolic rate after institution of a hypocaloric carbohydrate-free…diet…almost entirely reversed by isocaloric substitution of sucrose.”

Unfortunately, many studies are less than optimally designed, performed or interpreted. It’s possible that ulterior motives, agendas, or cognitive bias play a part. It is not popular to state that white sugar, fructose, or the saturated fats can provide protection against the inflammatory disease promoting things, even if results imply this to be the case.

Perhaps nobody wants to admit that it’s okay to have dessert before dinner, or for that matter, instead of dinner.

Replacing oils high in PUFAs, like soy, safflower, sunflower, canola, corn and fish oils, with coconut oil, butter, ghee and other highly saturated fats, can be a good starting point. A diet with enough protein from milk, cheese and gelatin and plenty of sugar from sweet fruits, fruit juice and white sugar is one potential way to help improve metabolic function and protect against stress and inflammation.

This is not so much a question of belief or non-belief. Experimentation and experience matter most. It’s better to find out for yourself.

See More Here

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

Orange juice or fructose intake does not induce oxidative and inflammatory response.

Glucose ingestion induces an increase in intranuclear nuclear factor kappaB, a fall in cellular inhibitor kappaB, and an increase in tumor necrosis factor alpha messenger RNA by mononuclear cells in healthy human subjects.

Potential role of endotoxin as a proinflammatory mediator of atherosclerosis.

Short term essential fatty acid deficiency in rats. Influence of dietary carbohydrates.

Mechanisms of Glucocorticoid-Induced Insulin Resistance

Sugar consumption, metabolic disease and obesity: The state of the controversy

12/15-Lipoxygenase Inhibition Reverses Cognitive Impairment, Brain Amyloidosis, and Tau Pathology by Stimulating Autophagy in Aged Triple Transgenic Mice.

Energy metabolism and lipid peroxidation of human erythrocytes as a function of increased oxidative stress.

TLR4 links innate immunity and fatty acid-induced insulin resistance.

Sucrose substitution in prevention and reversal of the fall in metabolic rate accompanying hypocaloric diets.

The health implications of changing linoleic acid intakes.

Inhibition of nuclear T3 binding by fatty acids.

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

Structural and functional rejuvenation of the aged brain by an approved anti-asthmatic drug

Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats.

Proinflammatory Effects of Hypoglycemia in Humans With or Without Diabetes

Diets rich in saturated and polyunsaturated fatty acids: metabolic shifting and cardiac health.

Insulin effects in muscle and adipose tissue.

Unsaturated fatty acids synergistically enhance glucocorticoid-induced gene expression.

Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis

UCP2 regulates mitochondrial fission and ventromedial nucleus control of glucose responsiveness

Moderately Reduced ATP Levels Promote Oxidative Stress and Debilitate Autophagic and Phagocytic Capacities in Human RPE Cells

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

Mitochondrial dysfunction and oxidative stress in aging and cancer

Inflammation Markers and Metabolic Characteristics of Subjects With 1-h Plasma Glucose Levels

Polyunsaturated fatty acids influence neonatal monocyte survival.

Arachidonic acid as a possible modulator of estrogen, progestin, androgen, and glucocorticoid receptors in the central and peripheral tissues.

Isoprostanes, Novel Eicosanoids That Produce Nociception and Sensitize Rat Sensory Neurons

High intake of saturated fat, but not polyunsaturated fat, improves survival in heart failure despite persistent mitochondrial defects

Postprandial Effect of a High-Fat Meal on Endotoxemia in Arab Women with and without Insulin-Resistance-Related Diseases

Medium-chain fatty acids: functional lipids for the prevention and treatment of the metabolic syndrome.

Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals.

Mechanisms of Insulin Resistance After Insulin-Induced Hypoglycemia in Humans: The Role of Lipolysis

Nitrogen conservation in starvation revisited: protein sparing with intravenous fructose.

Skeletal Muscle Insulin Resistance Promotes Increased Hepatic De Novo Lipogenesis, Hyperlipidemia, and Hepatic Steatosis in the Elderly

Endotoxemia is modulated by quantity and quality of dietary fat in older adults.

Lipid peroxidation products are elevated in fish oil diets even in the presence of added antioxidants.

Evidence-based review on the effect of normal dietary consumption of fructose on blood lipids and body weight of overweight and obese individuals.

Human Monocytes Engage an Alternative Inflammasome Pathway

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

Differential effects of fat and sucrose on the development of obesity and diabetes in C57BL/6J and A/J mice.

Fructose and galactose enhance postexercise human liver glycogen synthesis.

Saturated fatty acids suppress adrenocorticotropic hormone (ACTH) release from rat anterior pituitary cells in vitro.

High-fat meal induced postprandial inflammation.

Neuroendocrine perturbations as a cause of insulin resistance.

Glucocorticoid antagonism limits adiposity rebound and glucose intolerance in young male rats following the cessation of daily exercise and caloric restriction

Epoxy-keto derivative of linoleic acid stimulates aldosterone secretion.

Essential fatty acid-deficient diet modifies PAF levels in stomach and duodenum of endotoxin-treated rats.

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

Plasma malondialdehyde levels and risk factors for the development of chronic complications in type 2 diabetic patients on insulin therapy.

Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver

Dietary oxidized n-3 PUFA induce oxidative stress and inflammation: role of intestinal absorption of 4-HHE and reactivity in intestinal cells[S]

Linoleic acid induces proinflammatory events in vascular endothelial cells via activation of PI3K/Akt and ERK1/2 signaling.

Is glucose dysregulation an inflammatory process?

Plasma malondialdehyde levels and risk factors for the development of chronic complications in type 2 diabetic patients on insulin therapy.

Effects of a high-sucrose diet on body weight, plasma triglycerides, and stress tolerance.

Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.

Inflammation and insulin resistance

Oxidized products of linoleic acid stimulate adrenal steroidogenesis.

Consumption of carbohydrate solutions enhances energy intake without increased body weight and impaired insulin action in rat skeletal muscles.

Increase in intranuclear nuclear factor κB and decrease in inhibitor κB in mononuclear cells after a mixed meal: evidence for a proinflammatory effect

Linoleic acid: between doubts and certainties.

A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation.

Lipid Oxidation Products in the Pathogenesis of Inflammation-related Gut Diseases.

Maternal diet rich in omega-6 polyunsaturated fatty acids during gestation and lactation produces autistic-like sociability deficits in adult offspring.

Evidence for an inhibitor of extrathyroidal conversion of thyroxine to 3,5,3′-triiodothyronine in sera of patients with nonthyroidal illnesses.

Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis.

A High-Fat Diet Is Associated With Endotoxemia That Originates From the Gut

Daily Stressors, Past Depression, and Metabolic Responses to High-Fat Meals: A Novel Path to Obesity

High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects.

Pregnenolone protects mouse hippocampal (HT-22) cells against glutamate and amyloid beta protein toxicity.

Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials.

11β-HSD1 reduces metabolic efficacy and adiponectin synthesis in hypertrophic adipocytes.

Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.

Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog.

Marital Discord, Past Depression, and Metabolic Responses to High-Fat Meals: Interpersonal Pathways to Obesity

High Fat Diet-Induced Gut Microbiota Exacerbates Inflammation and Obesity in Mice via the TLR4 Signaling Pathway

Neutrophils support lung colonization of metastasis-initiating breast cancer cells

Replacing starch with sucrose in a high glycaemic index breakfast cereal lowers glycaemic and insulin responses.

Inhibition of chymase activity by phosphoglycerides.

Effect of long-chain fatty acids on the binding of thyroxine and triiodothyronine to human thyroxine-binding globulin.

Selective Inhibitors of 11β-Hydroxysteroid Dehydrogenase Type 1 for Patients With Metabolic Syndrome

Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes.

High rates of exogenous carbohydrate oxidation from a mixture of glucose and fructose ingested during prolonged cycling exercise.

Dietary intake of carbohydrates and risk of type 2 diabetes: the European Prospective Investigation into Cancer-Norfolk study.

Glucose Plus Fructose Ingestion for Post-Exercise Recovery—Greater than the Sum of Its Parts?

Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults.

Low Calorie Dieting Increases Cortisol

Insulin and glycemic responses in healthy humans to native starches processed in different ways: correlation with in vitro alpha-amylase hydrolysis.

Corn oil rapidly activates nuclear factor-κB in hepatic Kupffer cells by oxidant-dependent mechanisms

Diabetes and increased lipid peroxidation are associated with systemic inflammation even in well-controlled patients

Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis.



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