www.ClinicalTrials.govNCT01626742.

. Fatty liver in type 2 diabetes mellitus: relation to regional adiposity, fatty acids, and insulin resistance. Am J Physiol Endocrinol Metab 285: E906-E916, 2003; 10.1152/ajpendo.00117.2003.-The current study was undertaken to examine metabolic and body composition correlates of fatty liver in type 2 diabetes mellitus (DM). Eighty-three men and women with type 2 DM [mean body mass index (BMI): 34 Ϯ 0.5 kg/m 2 ] and without clinical or laboratory evidence of liver dysfunction had body composition assessments of fat mass (FM), visceral adipose tissue (VAT), liver and spleen computed tomography (CT) attenuation (ratio of liver to spleen), muscle CT attenuation, and thigh adiposity; these assessments were also performed in 12 lean and 15 obese nondiabetic volunteers. Insulin sensitivity was measured with a euglycemic insulin infusion (40 mU ⅐ m Ϫ2 ⅐ min Ϫ1 ) combined with systemic indirect calorimetry to assess glucose and lipid oxidation, and with infusions of [ 2 H2]glucose for assessment of endogenous glucose production. A majority of those with type 2 DM (63%) met CT criteria for fatty liver, compared with 20% of obese and none of the lean nondiabetic volunteers. Fatty liver was most strongly correlated with VAT (r ϭ Ϫ0.57, P Ͻ 0.0001) and less strongly but significantly associated with BMI (r ϭ Ϫ0.42, P Ͻ 0.001) and FM (r ϭ Ϫ0.37, P Ͻ 0.001), but only weakly associated with subcutaneous adiposity (r ϭ Ϫ0.29; P Ͻ 0.01). Fatty liver was also correlated with subfascial adiposity of skeletal muscle (r ϭ Ϫ0.44; P Ͻ 0.01). Volunteers with type 2 DM and fatty liver were substantially more insulin resistant those with type 2 DM but without fatty liver (P Ͻ 0.001) and had higher levels of plasma free fatty acids (P Ͻ 0.01) and more severe dyslipidemia (P Ͻ 0.01), a pattern observed in both genders. Plasma levels of cytokines were increased in relation to fatty liver (r ϭ Ϫ0.34; P Ͻ 0.01). In summary, fatty liver is relatively common in overweight and obese volunteers with type 2 DM and is an aspect of body composition related to severity of insulin resistance, dyslipidemia, and inflammatory markers.

Heme oxygenase (HO)-1 and its metabolic product carbon monoxide (CO) play regulatory roles in acute inflammatory states. In this study, we demonstrate that CO administration is effective as a therapeutic modality in mice with established chronic colitis. CO administration ameliorates chronic intestinal inflammation in a T helper (Th)1-mediated model of murine colitis, interleukin (IL)-10–deficient (IL-10 −/−) mice. In Th1-mediated inflammation, CO abrogates the synergistic effect of interferon (IFN)-γ on lipopolysaccharide-induced IL-12 p40 in murine macrophages and alters IFN-γ signaling by inhibiting a member of the IFN regulatory factor (IRF) family of transcription factors, IRF-8. A specific signaling pathway, not previously identified, is delineated that involves an obligatory role for HO-1 induction in the protection afforded by CO. Moreover, CO antagonizes the inhibitory effect of IFN-γ on HO-1 expression in macrophages. In macrophages and in Th1-mediated colitis, pharmacologic induction of HO-1 recapitulates the immunosuppressive effects of CO. In conclusion, this study begins to elucidate potential etiologic and therapeutic implications of CO and the HO-1 pathway in chronic inflammatory bowel diseases.

Prevention, early identification, and effective intervention are integral components of effective T2D care in Egypt. These strategies may reduce the expanding economic burden associated with T2D care.

Malnutrition is common across varying patient populations, particularly older adults, and sarcopenia prevalence increases with advancing age. Both malnutrition and sarcopenia are associated with substantial adverse outcomes affecting both the patient and the healthcare system, including increased morbidity, mortality, rehospitalization rates, and healthcare costs. Healthcare practitioners may assess patients for either malnutrition or sarcopenia; however, many patients clinically present with both conditions, resulting in the syndrome, Malnutrition-Sarcopenia Syndrome, which is the clinical presentation of both malnutrition and accelerated age-associated loss of lean body mass, strength, and/or functionality. Clinicians are urged to screen, assess, and treat these conditions currently so as to adequately address the full spectrum of patients' nutritional issues. By examining aspects of both conditions, clinicians can more fully assess their patients' clinical and nutritional status and can tailor targeted therapies to meet their needs and improve outcomes. This proposed syndrome embodies the inherent association of malnutrition and sarcopenia, highlighting their combined impact on clinical outcomes. The objective of this review paper is to characterize Malnutrition-Sarcopenia Syndrome to advance clinical practice, by providing clinicians with the necessary background information to integrate nutritional assessment along with loss of muscle mass and functionality in their everyday clinical practice.