On the Low Birth Weight Risk for Insulin Resistance

Altered PI3-Kinase/Akt Signalling in Skeletal Muscle of Young Men with Low Birth Weight
Original source: PLoS ONE 3(11): e3738
Authors: Christine B. Jensen, Malgorzata S. Martin-Gronert, Heidi Storgaard, Sten Madsbad, Allan Vaag, Susan E. Ozanne (corresponding author)
Publication date: November 17, 2008
DOI (digital document ID): 10.1371/journal.pone.0003738
Requires subscription? No
Publicly-available abstract: Yes

Synopsis:
Low birth weight (LBW), an indicator of stress or an adverse fetal environment, is associated with increased future risk of insulin resistance and type 2 diabetes. The investigators are reporting continuing research on a specific insulin signaling pathway may be altered in skeletal muscle of young adult men with LBW. This would help increase our understanding of the mechanisms of insulin resistance in this particular population.

Muscle biopsies were obtained from 20 healthy 19-yr old men who had been in the lowest 10% birth weight for full-term babies and compared them to 20 physically similar men of normal birth weight. The samples were checked for fasting blood glucose and insulin levels, and after four hours in which insulin-production was medically stimulated.

The researchers looked at several previously-unstudied proteins and pathways related to muscular function and muscular glucose metabolism to see if there was any difference between the two groups of men. They found significant differences in the levels of several proteins after insulin stimulation. Some of these differences seen in the LBW group are similar to those seen in patients with insulin-resistant Type 2 diabetes.

The authors conclude that these differences in skeletal-muscle response to insulin precede, and may contribute to, the development of whole-body insulin resistance and type 2 diabetes in men with LBW.


Reliability:
The tests were done on a small number of subjects and a small number of controls. The small sample could skew the results obtained. Also, these were spot observations. Longitudinal observation of these subjects (over a period of time) might give the researchers better information about whether or not insulin resistance progresses in this manner in these subjects.

Practical Applications:
This is one of a series in basic research of how diabetes may develop in specific populations.

In many areas, low birth weight is associated with maternal malnutrition and/or poor prenatal care -- which are further associated with low-income communities and minority communities. Type 2 diabetes is more common in these groups than in the general population. Proving a definite link and path may bring more interest in providing education, and medical and dietary services, to this high-risk group.

Ethics note:
Written informed consent was provided from all participants and approval was obtained from the regional ethics committee.

This synopsis was based on the entire article.

Iron-rich blood and metabolic syndrome

Hyperferritinemia Is Associated with Insulin Resistance and Fatty Liver in Patients without Iron Overload
Original source: PLoS ONE 3(10): e3547
Authors: Robert Brudevold (corresponding author), Torstein Hole, Jens Hammerstrøm
Publication date: October 28, 2008
DOI (digital document ID): 10.1371/journal.pone.0003547
Requires subscription? No
Publicly-available abstract: Yes

Synopsis:
Over the past ten years, the investigators have seen a rise in patients with hyperferritinemia (high blood ferritin) -- excess iron in the blood. A certain amount of this is to be expected given the increasing awareness of hereditary hemochromatosis -- a genetic condition in which the blood retains an overload of iron. High blood ferritin is also seen in cases of inflammation and in cancer. Over the same period, there has been an increase in patients whose high ferritin levels cannot be explained by these conditions. Most of these patients are overweight, middle-aged men.

Previous research suggested links between elevated ferritin levels and non-alcoholic fatty liver disease (NASH -- in technical terms, non-alcoholic steatohepatitis), and between high ferritin and insulin resistance. Both NASH and insulin resistance are often seen in patients with metabolic syndrome. The authors chose to examine this possible link in more detail.

They examined forty consecutive patients referred to them for hyperferritinemia. After examination, 34 patients remained with unexplained hyperferritinemia -- 1 woman and 33 men. Fasting blood samples were taken and analyzed for iron, liver enzymes, c-reactive protein (a marker for inflammation), and c-peptide (a marker for insulin production). Liver biopsies were obtained for 29 of the patients, and liver iron stores were assessed for 16 of them.

The majority of the patients had either markers for metabolic syndrome, or could be clinically diagnosed as having metabolic syndrome, showing increased body mass index, elevated diastolic blood pressure, and insulin resistance. Nineteen of the 29 patients biopsied had steatosis (fatty livers). Only four patients showed increased levels of iron in their livers -- of which two could be explained by alcohol consumption. Ferritin levels were higher in subjects with insulin resistance than in those without.

Fourteen of 16 patients normalized ferritin levels after phlebotomy (removal of an amount of blood -- a standard medical procedure for persons with hemochromatosis), but after a while, their ferritin levels rose again. Those who changed lifestyle (diet and exercise) -- first-line therapy for patients with metabolic syndrome -- had stabler ferritin levels. Since NASH is often seen in obese patients and in patients with metabolic syndrome, this evidence supports the theory associating NASH with increased ferritin levels.

These observations suggest that fatty livers and insulin resistance, but not increased iron storage in the liver, may be frequently seen in patients referred to specialists because of high ferritin levels. The authors conclude that ferritin levels seem to be higher in people with insulin resistance and suggest that high ferritin levels are markers of metabolic syndrome with NASH and insulin resistance, rather than iron overload.

Reliability:
There were very few subjects examined in this study, and no indication of how common this complaint is within the population affected by insulin resistance and/or metabolic syndrome. Because of this, there is a possibility of skewed data.

The tests support previous research, adding information to the existing body of knowledge and suggesting directions for further research.

The authors are associated with accredited medical institutions and the article is published in a peer-reviewed journal.

Practical Applications:
Understanding the entire extent of physiological changes associated with metabolic syndrome can help doctors and pharmacists better understand both metabolic syndrome in general and how best to treat the individual patients.

While the population studied is small, it supports our understanding that lifestyle management -- maintenance of a stable, healthy weight through diet and exercise -- is of vital importance for maintaining or improving our overall health.

Ethics note: All patients gave oral consent to the examination program and to the use of clinical data for research purposes.

This synopsis was based on the entire article.

Can fish oil counteract sleep deprivation?

Dietary fish oil did not prevent sleep deprived rats from a reduction in adipose tissue adiponectin gene expression
Original source: Lipids in Health and Disease 2008, 7:43
Authors: Ana BM Mattos, Monica JS Pinto, Cristiane Oliveira, Carolina Biz, Eliane B Ribeiro, Claudia M Oller do Nascimento, Monica L Andersen, Sergio Tufik, and Lila M Oyama (corresponding author)
Publication date: 5 November 2008
DOI (digital document ID): 10.1186/1476-511X-7-43
Requires subscription? No
Publicly-available abstract: Yes

Synopsis:
Sleep deprivation has been one of the hallmarks of modern society. Where it was once limited to the elderly, now even youth are chronically sleep deprived. Sleep deprivation is linked to adverse metabolic effects, including insulin resistance. Omega-3 fatty acids found in fish oil have been seen to improve insulin sensitivity -- decrease insulin resistance. We don't yet know how this works, but researchers believe that adiponectin has a role.

The aim of this study is to assess the effects of diets high in fish oil on sleep-deprived subjects. The authors note that while in humans, sleep deprivation is associated with weight gain, sleep-deprived rats tend to lose weight. This suggests to them a method of measuring insulin resistance in such a way that it is not related to weight gain. Glucose tolerance, serum insulin, and adiponectin levels are examined in both sleep-deprived and non-sleep-deprived rats.

The rats were kept awake for 96 hours, which is when the most dramatic alterations in lipid and hormone concentrations occur. At that time, the rats were subjected to a glucose tolerance test, starting with blood drawn after a 12-hour fast, and then after the glucose was given, at time intervals of 4, 12, 20, 24, 28 and 32 minutes. The blood sampled was tested for glucose concentration, insulin, and adiponectin levels. The animals were then killed, weighed, and the fat and protein contents of their bodies separated and measured. Adiponectin and transfer-RNA were measured from the animals' adipose tissues.

Sleep deprivation caused the rats to lose weight whether or not they were on fish-oil-rich diets (this is normal for rats). Non-sleep-deprived rats did not lose weight. Sleep-deprived rats fed a normal diet lost fat; those fed a fish-oil-rich diet did not. No change was observed in protein content of any of the groups.

Following the glucose tolerance tests, glucose concentration was significantly higher in the rats allowed to sleep than those who were sleep-deprived -- and in the last measurement, the glucose level in the rats who were both sleep-deprived and fed a fish-oil-rich diet dropped even further relative to the other groups.

Serum insulin and adiponectin was similar across all groups; however, the gene expression of adiponectin in abdominal tissue was lower in the sleep-deprived rats than the non-sleep-deprived rats. Insulin levels were lower in sleep-deprived male rats, so there may have been unaccounted-for factors in the test.

The authors examine the findings of previous studies on lipid consumption, fish oil, sleep deprivation, and adiponectin expression in rats to put their study into context. They conclude that sleep deprivation does cause a stress-related drop in adiponectin gene expression, which negatively effects insulin sensitivity.


Reliability:
There were only 5-9 rats per group studied. This is a very small sample, in which results can be skewed. Rats may not be a good model for humans in this environment, as humans tend to gain weight when sleep-deprived and there are perceived correlations between weight gain and insulin sensitivity. The readings for the rats were taken at the point of peak change of a single episode of sleep deprivation, rather than after a long period of chronic sleep deprivation (e.g., 1 month at 2 hrs less sleep than normal mice get). This is the difference between students spending a couple of all-nighters cramming for an exam versus a young professional working sixteen-hour days for several years to establish himself in a competitive field.

Practical Applications:
If it could be proven that fish oil supplements (or a diet rich in fish) could protect humans against some of the adverse metabolic effects of sleep deprivation, then this could be an effective and inexpensive treatment against those medical risks.

This synopsis was based on the entire article.

Can metformin help Type 1 diabetics?

Effect of Adjunct Metformin Treatment in Patients with Type-1 Diabetes and Persistent Inadequate Glycaemic Control. A Randomized Study
Original source: PLoS ONE 3(10): e3363
Authors: Søren Søgaard Lund (corresponding author), Lise Tarnow, Anne Sofie Astrup, Peter Hovind, Peter Karl Jacobsen, Amra Ciric Alibegovic, Ida Parving, Lotte Pietraszek, Merete Frandsen, Peter Rossing, Hans-Henrik Parving, Allan Arthur Vaag
Publication date: October 9, 2008
DOI (digital document ID): 10.1371/journal.pone.0003363
Requires subscription? No
Publicly-available abstract: Yes

Synopsis:
Despite intensive insulin use, many people who have had Type 1 (autoimmune) diabetes for a long period of time have trouble maintaining adequate glucose control and achieving an HbA1c of under 7%, which is considered a threshold beneath which the risk of developing complications of diabetes is reduced. There are a number of reasons -- physiological (medical), environmental, and psychological -- for poor control. One of the physiological reasons may be the development of insulin resistance over time. This study looks at the potential for adding the use of metformin -- an initial drug of choice in treating Type 2 (metabolic) diabetes (which often includes insulin resistance) -- to the use of insulin to improve blood glucose control in Type 1 diabetes.

The study included 100 Type 1 diabetes patients with poorly-controlled blood glucose levels (defined as HbA1c over 8%). A one-month period in which all of them received identical placebo pills was followed by a three-week period in which the pills of half of the patients was gradually changed to include 1000 mg metformin, twice daily. The other patients continued to receive placebo pills. The patients were followed at one- to three-month intervals, for a period of a year after maximum/target dose was achieved.

The study was conducted as a double-blind study, which means that neither the investigators nor the patients knew who was taking metformin and who was not.

At each clinic visit before and during the study, patients were tested for HbA1c, c-peptide levels (a protein used as an indicator of remaining beta-cell function), and blood glucose level. Their body mass index (BMI -- a comparison of weight to height) was also measured. They were asked to estimate the average of the blood glucose measurements they took themselves at home. They were also requested to report serious adverse effects (including life-threatening events requiring hospitalization, or which resulted in persistent or significant loss of physical abilities, or which caused an adverse reaction due to a birth defect, and hypoglycemic events which resulted in unconsciousness or which required the intervention of a third party) and minor adverse effects (including hypoglycemia mild enough for the patient to be able to treat himself). They were also asked to report any changes to their insulin prescriptions and treatments (change of type of insulin, number of injections per day, sites used, and dosage).

In addition to analyzing the HbA1c measurements of the entire groups (metformin and placebo), researchers counter-checked changes in HbA1c with changes in patient weight and insulin dosage. They also analyzed the measurements from overweight and obese patients separately from those of normal weight, and the results from those taking higher amounts of insulin daily from those taking smaller amounts, since insulin resistance is often treated with higher doses of insulin; it is also associated with overweight and obesity.

The results of the analysis showed no significant changes in HbA1c level for either group. However, the metformin users lost, on average, a little more than a kilogram of body weight and were able to reduce their daily insulin usage by, on average, 0.03 units per kilogram of body weight. By comparison, those patients on placebo did not lose weight and, on average, needed to increase their insulin usage by 0.03 units per kilogram of body weight. (This corresponds to average total daily insulin use of 3 units less per day for the metformin group, and about 2.5 units more per day for the placebo group.)

The results of this study were compared to the results of previous studies, and the strengths and limitations of both this study and those were examined.

Reliability:
The authors are professionals in the fields of endocrinology and diabetes care, associated with accredited institutions. The results were published in a peer-reviewed journal.

The study size was small, so there is some potential for skew.

The use of double-blinding and placebos removed the variables of being able to attribute all good effects to the use of the drug, as well as that of all positive effects being due to the suggestion of the pills being effective.

The duration of the study was long enough to determine whether metformin would have any effect on HbA1c; however, the reduction in insulin use among the metformin patients may have counteracted the drug's effects on lowering HbA1c. The authors note that had they specified that the patients not drop their insulin dosages, there may have been a greater risk of serious hypoglycemic events.

Practical Applications:
The authors suggest that the mild weight reduction and apparent improved insulin sensitivity among the patients treated with metformin may lower these patients' diabetes-related cardiovascular risks; however, metformin does not appear to be a useful tool for improving glycemic control in patients with long-duration Type 1 diabetes.


This synopsis was based on the entire article.

Are moderate-protein diets better than low-protein diets for people with metabolic syndrome?

Moderate carbohydrate, moderate protein weight loss diet reduces cardiovascular disease risk compared to high carbohydrate, low protein diet in obese adults: A randomized clinical trial

Original source: Nutrition & Metabolism 2008, 5:30
Authors: Denise A Walker Lasker (corresponding author), Ellen M Evans, and Donald K Layman
Publication date: 7 November 2008
DOI (digital document ID): 10.1186/1743-7075-5-30
Requires subscription? No
Publicly-available abstract: Yes

Synopsis:
This study compares the effectiveness of the standard USDA Food Pyramid diet with a higher-protein, lower-carbohydrate diet for weight loss in general, for fat loss in particular, and for lowering the blood-based indicators of cardiovascular risk and insulin resistance. A total of 50 people completed the testing, split between the two dietary approaches.

Both diets under test had the same amount of calories, with about 30% of total calories coming from fats. Carbohydrates supplied about 55% of the Food Pyramid diet group's caloric intake, and protein, the remaining 15%. The people assigned to this group were instructed to eat whole grains for their bread products. About 30% of the high-protein group's calories came from protein, with the remaining 40% coming from carbohydrates. (This is the same protein-carbohydrate-fat distribution advocated by the Zone Diet.) This group was instructed to eat primarily "high quality protein", including lean meats, dairy, and eggs. Both groups had similar amounts of fruits and vegetables in their daily diets. All subjects were instructed on portion sizes, dietary substitutions, how to weigh foods, and how to keep a food diary. There was no difference in exercise between the two groups.

Baseline measurements (weight, body fat percentage, cholesterol, and postprandial insulin) were taken at the start of the experiment. The subjects followed their assigned diet plans for four months, at which time the same measurements were repeated.

• The moderate-protein group lost about 5 pounds more per person than the USDA group, and more of their weight loss was from fatty tissues.
• Fasting glucose levels were unchanged, but fasting insulin levels decreased in the moderate protein group, while it increased in the USDA group. In addition, postprandial insulin levels dropped 85% for the protein group, but only 50% for the Food Pyramid group. (High plasma insulin levels are indicative of insulin resistance, which is often a predecessor to Type 2 diabetes.)
  
• There was a greater drop in total cholesterol in the USDA group than in the protein group. LDL ("bad") cholesterol dropped in the USDA group but rose in the protein group; on the other hand, HDL ("good") cholesterol dropped in the USDA group but rose in the protein group. The protein group also showed greater improvement in triglyceride levels than the USDA group. (High triglyceride levels are associated with increased risk of heart attack.)
  

Reliability:
The study was small scale, with only 50 people completing the four-month study. While the two groups of subjects were selected to be closely-matched, there is still opportunity for the results to be skewed. An initial run-in period put all subjects on as close to an even footing as possible before the trial started.
The authors are associated with an accredited university; the paper was published in a peer-reviewed journal.
Longer-term studies of larger groups may be needed to determine the long-term safety and effectiveness of high-protein diets.

The principal investigator (Denise A Walker Lasker) received funding from the National Cattleman’s Beef Association, The Beef Board and Kraft Foods. Both Beef associations have a vested interest in increasing protein consumption (in the form of beef).
The investigators have made no comparison between a higher-fat restricted-carbohydrate diet and a higher-protein restricted-carbohydrate diet.

Practical Applications:
The 30/40/30 protein/carb/fat (PCF) ratio is the basis of the Zone Diet. While this diet is higher in protein than traditionally advised for people with diabetes, recent publications suggest that this is not as high a risk as formerly perceived.

For further reading:
WebMD evaluates the Zone Diet
Wikipedia entry on the Zone Diet

This synopsis was based on the entire article.

Prenatal diet may affect insulin resistance for multiple generations

Insulin sensitivity is normalized in the third generation (F3) offspring of developmentally programmed insulin resistant
(F2) rats fed an energy-restricted diet
Original source: Nutrition and Metabolism 2008, 5:26
Authors: Daniel C Benyshek (corresponding author), Carol S Johnston, John F Martin and William D Ross
Publication date: 17 October 2008
DOI (digital document ID): 10.1186/1743-7075-5-26
Requires subscription? No
Publicly-available abstract: Yes

Synopsis:
A number of studies have shown that the way animals develop before birth can affect the birth weights, blood pressure, and glucose metabolisms of their children, grandchildren, and so on. Most research to date has only gone two generations beyond the original parents. This study takes observation to the third generation (great-grandchildren) and focuses on impairments to the animals' glucose metabolisms. A parent generation of female rats were fed protein-deficient diets while pregnant and nursing, and both they and three generations of their offspring were fed low-calorie diets, to see how this affected the insulin sensitivity of multiple generations of their offspring. A group of control rats was fed normal-calorie diets over the same number of generations.

The first generation of offspring (children) tended to be of low birth weight, while the second and third generations (grandchildren and great-grandchildren) were of normal birth weight. All generations were of lower than normal weight as adults, due to the caloric restriction. The first=generation offspring had normal insulin metabolism, While the second generation, as adults, had reduced insulin sensitivity and reduced insulin production -- a set of symptoms consistent with impaired glucose tolerance. The third generation did not show insulin resistance -- indeed, the males were even more insulin-sensitive than the control animals, whether they were fed calorie-restricted diets or allowed to eat at will.

Previous studies of this type showed insulin resistance in the first-generation offspring, which was not found in this particular study; however, the second-generation female offspring in this study were insulin-resistant.

The investigators are unsure why the third-generation offspring did not show impaired glucose tolerance or insulin resistance, even though both of those traits are considered to be adaptive traits that show up in "nutrient poor environments" (reduced protein, reduced calories). They suggest that one reason for this may be that the second-generation mother's insulin resistance left more energy in the bloodstream to be used by the fetus. On the other hand, the relative insulin sensitivity of previous-generation mothers (who had not been fed sufficient calories after weaning) made fewer nutrients available for the developing fetus, resulting in insulin resistance in the offspring.

The investigators suggest that more research is required to determine how pregnancy and nursing diets, and maternal insulin sensitivity, affects the insulin sensitivity of her offspring.

Reliability:
The authors are from accredited institutions, across a number of medical and social disciplines. The research was published in a peer-reviewed online journal. References are all from peer-reviewed journals. Therefore the experiment design is reliable. Since only four female rats from each child generation were bred, the study was small in size and therefore subject to skew. The authors did note that further research was warranted to find out why they got the results they did.

Practical Applications:
The normal birth weight and increased insulin sensitivity of child generations born to insulin-resistant mothers suggests a parallel mechanism for the large baby size common for human mothers with diabetes. While this study was conducted on rats, the rats are intended to be a shorter-lived and expendable model for human childbirth and development. A closer understanding of which maternal nutrients affect insulin resistance may lead to improved recommendations for pregnancy and nursing diets and supplements, and will ideally prevent insulin resistance in future generations of human adults.

This synopsis was based on the entire article.

A possible reason for increased risk of infection of obese people and those with Type 2 diabetes

Interleukin-18 resistance in patients with obesity and type 2 diabetes mellitus
Original source: International Journal of Obesity (2008) Vol. 32, pp. 1407–1414
Authors: G R C Zilverschoon, C J Tack, L A B Joosten, B J Kullberg, J W M van der Meer and M G Netea (corresponding author)
Publication date: published online 22 July 2008
DOI (digital document ID): doi:10.1038/ijo.2008.109
Requires subscription? Not for this article
Publicly-available abstract: Yes

Synopsis:
Interleukin-18 (IL-18) is a signalling chemical (similar to hormones) that has a strong effect on stimulating interferon (IFN) release. It is produced by a number of different white blood cells and central nervous system cells. Interferon is an important chemical in fighting infections.

Higher levels of IL-18 have been shown to decrease abnormally large appetite and to improve insulin sensitivity. Interestingly, several studies have shown high levels of IL-18 in obese people with insulin resistance, and a recent study has demonstrated that a common version of the genes producing IL-18 is associated with a higher body mass index (weight) in people with type 2 diabetes or coronary heart disease. In addition, weight loss after bariatric surgery (such as gastric bypass or lapband) results in lowered blood concentrations of IL-18.

The investigators suspect that the cells of obese people and those with insulin resistant diabetes may have high levels of IL-18 because they do not respond as well to IL-18 as those of people of normal weight and who are not diabetic. To test this theory, they tested white blood cells of obese and Type 2 diabetes patients and compared them to those of lean, non-diabetic people, and measured their IFN production in relation to their IL-18 levels. They found that in the obese and the diabetic subjects, these cells respond poorly to IL-18 and produce less interferon. They also show impaired release of IFN after exposure to disease-carrying bacteria and fungi.

They conclude that the reduced response to IL-18 may be responsible for the increased susceptibility to infection among those who are obese or who have Type 2 diabetes.

Reliability:
The study was conducted with a small number of subjects: seventeen control subjects, eleven obese non-diabetic subjects, and fourteen subjects with Type 2/insulin-resistant diabetes. (The possibility of LADA or other autoimmune diseases was ruled out at the start of the study.) The smaller the number of subjects, the greater the possibility for skewed or atypical results. The research was published in a peer-reviewed journal, and the investigators are all associated with the a University Medical Center in the Netherlands. Based on the small number of subjects, the results should be considered to point in the direction of larger studies to confirm the investigators' results, as well as further research into why these cells have an impaired reaction to IL-18.

Practical Applications:
A confirmed pathway and reason for increased risk of infection among obese people and people with Type 2 diabetes could lead to therapy to reduce that risk and to better fight those infections that do occur. If insulin resistance and excessive appetite are also directly related to impaired IL-18 response, then improving that response could conceivably result in weight loss and improved insulin sensitivity as well.


This synopsis was based on the entire article.

Investigating Insulin Resistance in the Liver

Inhibition of cytohesins by SecinH3 leads to hepatic insulin resistance
Authors: Markus Hafner, Anton Schmitz, Imke Grüne, Seergazhi G. Srivatsan, Bianca Paul, Waldemar Kolanus, Thomas Quast, Elisabeth Kremmer, Inga Bauer and Michael Famulok
Original source: Nature Volume 444, pp. 941-944
Publication date: 14 December 2006
DOI (digital document ID): doi:10.1038/nature05415
Requires subscription? For complete article
Publicly-available abstract: Yes

Synopsis:
G proteins regulate biochemical "switches" in all living systems. They are switched on and off by chemicals called "guanine nucleotide exchange factors" or GEFs. Finding chemicals which increase or inhibit GEFs may be useful both to find out how GEFs work and to treat diseases in which the G proteins are affected.

A specific class of GEFs called "cytohesins" includes some GEFs that are associated with insulin production and signalling. The investigators found that in humans, a chemical called "SecinH3" might inhibit the cytohesins associated with insulin signalling. To test this theory, mice were treated with SecinH3 and observed to determine whether or not they showed increased signs of insulin resistance.

The mice exhibited increased glucose production, reduced glycogen storage and glycogen-to-glucose conversion, a reduced ability to metabolize fatty acids and ketones, and increased plasma insulin. These are all symptoms of insulin resistance, suggesting that increased levels of SecinH3, and/or decreased activity of cytohesins, may be responsible for insulin resistance.

The importance of this finding is that insulin resistance is one of the first signs of Type 2 diabetes.

Reliability:
The initial hypothesis was based on the isolation of SecinH3 and its effects in isolated human liver tissue, so even though this experiment took place in mice, it has a good probability of being directly transferrable to people. The article was published in a peer-reviewed journal, and the authors are professional researchers in biochemistry and immunology.
This leads to high confidence in the results.

Practical applications:
This research is still very early on in the process of developing new treatments for insulin resistance and Type 2 Diabetes.

This synopsis was based on the abstract only.