1. Dietary fat may contribute to insulin resistance. From one review:
"Overall, most animal and cell studies seem to indicate that saturated and trans-unsaturated fatty acids significantly increase insulin resistance."2. Dietary fat contains some of the highest levels of Persistant Organic Pollutants of the foods we eat.
- Skeletal Muscle Lipid Deposition And Insulin Resistance: Effect Of Dietary Fatty Acids And Exercise, American Journal of Clinical Nutrition, 2007
This study found that people with high levels of POPs were 38 times! more likely to have diabetes than those with low levels:3. Dietary fat contributes to inflammation. One way it does so is by increasing absorption of endotoxins, to which we launch an inflammatory response. Chronic inflammation is linked to insulin resistance, diabetes, and other elements of the Metabolic Syndrome. Also, endotoxins by themselves (independent of inflammatory markers) have been linked to diabetes. (Endotoxins are bits of bacterial membrane that are absorbed along with the fat we eat. They're thought to derive, in part, from bacteria that live in the intestines.)
A Strong Dose-Response Relation Between Serum Concentrations Of Persistent Organic Pollutants [POPs] And Diabetes: Results From The National Health And Examination Survey 1999–2002, Diabetes Care, 2006
Here's just one recent study on the topic of endotoxins. This is a hot area right now:
High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects, Diabetes Care, Online December 2011
"Ingestion of a high-fat meal led to a significant rise in endotoxin levels in type 2 diabetic, IGT [impaired glucose tolerance], and obese subjects over the 4-h time period (P < 0.05). These findings also showed that, at 4 h after a meal, type 2 diabetic subjects had higher circulating endotoxin levels (125.4%↑) than NOC [nonobese control] subjects (P < 0.05).And a study that links dietary fat, specifically saturated fat, to inflammation:
These studies have highlighted that exposure to a high-fat meal elevates circulating endotoxin irrespective of metabolic state, as early as 1 h after a meal. However, this increase is substantial in IGT and type 2 diabetic subjects, suggesting that metabolic endotoxinemia is exacerbated after high-fat intake."
Acute And Chronic Saturated Fatty Acid Treatment As A Key Instigator Of The TLR-mediated Inflammatory Response In Human Adipose Tissue, Journal of Nutritional Biochemistry, January 2012
"[Our] data highlights the potential risk of a continued high fat diet on inducing an inflammatory response, as it appears to be more pronounced than the glucose induced response. This would also appear to align with clinical studies that suggest hyperlipidaemia may impact more significantly over time than hyperglycaemia in the pathogenesis of metabolic disease.
This study implicates elevated SFAs [saturated fatty acids] as a key instigator of the inflammatory response."
Saturated fat seems to be the riskiest type.