ABSTRACT
Acknowledgments......................................................................................................................... 430
References..................................................................................................................................... 431
Diabetes mellitus is defined by increased blood glucose (hyperglycemia) in the fasted and/or in the
postprandial state [1]. Hyperglycemia is a consequence of inappropriate insulin secretion by
pancreatic b cells due to autoimmune destruction in type 1 diabetes mellitus (T1DM) or rare
inherited defects in maturity onset diabetes of the young (MODY). The most frequent diabetes type,
type 2 diabetes mellitus (T2DM), is primarily due to impaired insulin action, i.e., insulin resistance,
at its target tissues such as skeletal muscle, liver, and adipose tissue [1]. Insulin resistance is usually
linked to increased visceral fat mass, arterial hypertension, hyperuricemia, dyslipidemia, and
endothelial dysfunction, which are summarized as term pluri or dysmetabolic syndrome [2]. These
abnormalities are also found in women who develop glucose intolerance during pregnancy, i.e.,
gestational or type 4 diabetes mellitus (T4DM). The dysbalance of energy homeostasis with caloric
intake exceeding energy expenditure is currently held responsible for the epidemic spread of
obesity and diabetes [3,4]. Abnormalities of fat distribution such as lipodystrophy also lead to
severe insulin resistance and diabetes [5]. With in vivo MRS, clinical studies became feasible for
the detailed investigation of the pathophysiology and therapeutic options in human diabetes
mellitus.
