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James Cramer (NY Magazine): How to Withstand the Coming Bush Economic Crisis. For the longest time, because Bush is a Republican, we on Wall Street simply didn�t believe that he could be a reckless spender. We knew only two paradigms: You either spent less and cut taxes or you spent more and raised taxes. Both courses at least presumed some sacrifice at some time. Not Bush�s plan. He�s gone on both the biggest spending binge and the lowest taxation course in U.S. history, which, alas, will produce gigantic liabilities down the road. Of course, he�ll be back on the ranch by the time his successor will have to deal with his inflation and currency debasement. Our only hope that financial disaster won�t strike sooner lies with the Chinese, who actually fund our deficit by buying our Treasuries�$242 billion worth, or 12 percent of all foreign holdings. If the Chinese decide to be good communists and stop buying our bonds, the Feds will have to raise rates to attract new investors and the reaper will be at our doorstep with interest rates more akin to those of South than North America. Right now, it�s not a problem. But in a year or two or maybe less, I perceive that the government will throw a bond auction and nobody will show, including the Chinese, until rates shoot up dramatically.

interesting is nt it

“First they ignore you. Then they laugh at you. Then they fight you. Then you win.” Mohandas Gandhi

Type 2 Diabetes: Insulin Resistance May Be the Result of Mitochondrial Dysfunction

DOI: 10.1371/journal.pmed.0020292

Published: August 16, 2005

Copyright: � 2005 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Public Domain Declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

Citation: (2005) Type 2 Diabetes: Insulin Resistance May Be the Result of Mitochondrial Dysfunction. PLoS Med 2(9): e292

The role of insulin resistance (IR) in type 2 diabetes, the most frequently encountered metabolic disorder in the world, has attracted much attention in recent years. Virtually all patients with type 2 diabetes have IR, which usually appears some 10�20 years before the disease itself. Although the existence of the relationship between IR and type 2 diabetes is well recognized, the underlying mechanisms are poorly understood. A study by Kitt Falk Petersen and colleagues provides important new information on the underlying pathogenic mechanisms that lead to the development of IR.

Recent findings have suggested that inherited defects in mitochondrial oxidative phosphorylation activity might play a key role in the development of IR. Studies have demonstrated a relationship between dysregulated fatty acid metabolism, fat accumulation in muscle cells, and IR in skeletal muscle. This fat accumulation appears to interfere with insulin signaling, resulting in reduced insulin-stimulated muscle glucose transport activity and decreased muscle glycogen synthesis. Magnetic resonance spectroscopy (MRS) studies have found reduced basal rates of muscle mitochondrial ATP production, associated with increased intramyocellular lipid content. Consistent with these results, microarray studies have found a coordinated reduction in PGC-1�-responsive genes in patients with obesity and type 2 diabetes and their overweight first-degree relatives.

Building on these findings, Petersen and colleagues examined insulin-stimulated rates of muscle ATP synthesis and phosphate transport, to investigate whether mitochondrial function is affected not only in the fasting state but also during insulin stimulation and to determine whether inherited defects in mitochondrial oxidative phosphorylation activity might be responsible for IR.

Participants in the study were in their late 20s, lean, nonsmoking individuals with IR who were offspring of parents with type 2 diabetes. The participants were thus selected to be free of other risk factors for IR such as obesity and smoking. Such individuals are ideal for examining the earliest metabolic defects responsible for the pathogenesis of IR since they have none of the confounding factors that are likely to be present in patients with type 2 diabetes. A metabolic defect in this group is likely to be an early event of genetic origin and, therefore, is potentially a primary cause of the later development of diabetes. The individuals in the control group were healthy, nonsmoking, and matched for age and weight to the individuals in the IR group. Insulin was administered using a hyperinsulinemic-euglycemic clamp, and rates of mitochondrial phosphorylation activity (muscle ATP synthesis) were assessed by MRS.
Mitochondria in human muscle cell

Rates of insulin-stimulated glucose uptake were decreased by approximately 50% in the individuals with IR compared to the controls and were associated with an approximately 2-fold increase in intramyocellular lipid content. In the control individuals, rates of ATP synthesis increased by approximately 90% during the hyperinsulinemic-euglycemic clamp. In contrast, insulin-stimulated rates of muscle mitochondrial ATP synthesis increased by only 5% in the individuals with IR. This small increase in muscle mitochondrial ATP synthesis in the individuals with IR was associated with a severe reduction of insulin-stimulated increases in intramyocellular phosphorus concentrations.

The authors say their study provides further evidence that IR in skeletal muscle of individuals with IR who are offspring of parents with type 2 diabetes may be related to defects in mitochondrial dysfunction. Furthermore, there were also severe defects in insulin-stimulated phosphate transport into skeletal muscle in the individuals with IR, which may be part of the defect leading to impaired ATP synthesis in the muscle of these individuals.

The implications of the study are also discussed in a Perspective by Anton Wagenmakers (DOI: 10.1371/journal.pmed.0020289). Although he suggests that the defects underlying IR are likely also to involve organs other than muscle, he notes the clinical relevance of the main finding, which might explain the weight maintenance problems that individuals with obesity and IR have.

Mother’s Stress May Trigger Child’s Diabetes: “ Type 1 diabetes arises when the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. What triggers this autoimmune reaction isn’t clear. But new research indicates that children of women who experience stressful adverse life events appear to be prone to develop type 1 diabetes.

Results of a Swedish study, involving nearly 6000 children and their families, shows that mothers’ experience of divorce or violence raised the risk of diabetes-related autoimmunity in children at age 2.5 years by roughly threefold. The research is published in the current issue of the journal Diabetes Care.

The thinking is that kids become stressed too, raising their level of the stress hormone cortisol, which may lead to insulin resistance.

Summary of the study available here. 

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