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Increased hepatic glucose output and decreased glucose utilization are implicated in the development of type 2 diabetes. We previously reported that the expression of a novel gene, Tanis, was upregulated in the liver during fasting in the obese/diabetic animal model Psammomys obesus. Here, we have further studied the protein and its function. Cell fractionation indicated that Tanis was localized in the plasma membrane and microsomes but not in the nucleus, mitochondria, or soluble protein fraction. Consistent with previous gene expression data, hepatic Tanis protein levels increased more significantly in diabetic P. obesus than in nondiabetic controis after fasting. We used a recombinant adenovirus to increase Tanis expression in hepatoma H4IIE cells and investigated its role in metabolism. Tanis overexpression reduced glucose uptake, basal and insulin-stimulated glycogen synthesis, and glycogen content and attenuated the suppression of PEPCK gene expression by insulin, but it did not affect insulin-stimulated insulin receptor phosphorylation or triglyceride synthesis. These results suggest that Tanis may be involved in the regulation of glucose metabolism, and increased expression of Tanis could contribute to insulin resistance in the liver., A major factor that contributes to hyperglycemia in type 2 diabetes is excessive hepatic glucose production. Depending on the concentrations of insulin and glucagon in the portal blood and the [...]

ROBERT D. LINDEMAN, MD [1,2] LINDA J. ROMERO, MD [2,3] ASENATH LARUE, PHD [2,4] C. LILLIAN YAU, MS [2] DAVID S. SCHADE, MD [1] KATHLEEN M. KOEHLER, PHD [2] RICHARD [...]

IRINA KOWALSKA, MD [1] JOLANTA PROKOP, MD [2] HANNA BACHORZEWSKA-GAJEWSKA, MD [2] BEATA TELEJKO, MD [1] IDA KINALSKAL, MD [1] WACLAW KOCHMAN, MD [3] WLODZIMIERZ MUSIAL, MD [2] Postload glycemia [...]

JIMMY P.S. CHERN, MD [1] KAI-HSIN LIN, MD [2] MENG-YAO LU, MD [2] DONG-TSAM LIN, MD [2] KUO-SIN LIN, MD, PHD [2] JONG-DAR CHEN, MD [1] CHENG-CHUNG FU, MD [1] [...]

The presence of tumors places rigorous metabolic demands on the host and the growing tumor poses a stress on the host to maintain normal blood glucose levels. Hepatic glucose-6-phosphatase (G6Pase) [...]

We sought to determine if variation in genes influencing insulin action and/or secretion contribute to the high prevalence of glucose intolerance in women with polycystic ovary syndrome (PCOS) and their [...]

To directly assess the role of ATP-sensitive K ([K.sub.ATP]) channel in glucosestimulated insulin secretion we made and characterized type 1 sulfonylurea receptor (Sur1) knock-out (Sur1 KO) mice. Formation of functional [...]

Hyperglycemia of diabetes, is caused in part by perturbation of hepatic glucose metabolism. Hepatic glucokinase (GK) is an important regulator of glucose storage and disposal in the liver. This project [...]

Brain glycogen is an endogenous store of carbohydrates that can serve as a fuel during hypoglycemia. In most tissues, glycogen (Glyc) has been shown to replete to levels higher than [...]

The increased risk of hypoglycemia during intensified treatment of type 1 diabetes (T1DM) is attributed to suppressed adrenomedullary responses. A consequence of this impairment of catecholamine secretion might be reduced [...]

Salicylate treatment has previously been demonstrated to improve oral glucose tolerance in diabetic rats and humans. In order to examine the mechanism by which this occurs, insulin-stimulated glucose metabolism and [...]

The current WHO diagnostic criteria for diabetes mellitus (DM) and other categories of hyperglycemia classify abnormal glucose tolerance according to elevated blood glucose concentrations in either the fasting or postload [...]

Background: The role of gluconeogenesis from protein in the pathogenesis of weight loss in lung cancer is unclear. Objective: Our aim was to study gluconeogenesis from alanine in lung cancer patients and to analyze its relation to the degree of weight loss. Design: In this cross-sectional study, we used primed-constant infusions of [6,6-[sup.2][H.sub.2]]-D-glucose and [3-[sup.13]C]-L-alanine to assess whole-body glucose and alanine turnover and gluconeogenesis from alanine in weight-losing (WL, n = 9) and weight-stable (WS, n = 10) lung cancer patients and healthy control (n = 15) subjects. Results: Energy intake and plasma alanine concentrations did not differ significantly among the subject groups. Mean ([+ or -] SEM) whole-body glucose production was significantly higher in WL than in WS and control subjects (0.74 [+ or -] 0.06 compared with 0.55 [+ or -] 0.04 and 0.51 [+ or -] 0.04 mmol [multiplied by] [kg.sup.-1] [multiplied by] [h.sup.-1], respectively, P [is less than] 0.01). Alanine turnover was significantly elevated in WL compared with WS and control subjects (0.57 [+ or -] 0.04 compared with 0.42 [+ or -] 0.05 and 0.40 [+ or -] 0.03 mmol [multiplied by] [kg.sup.-1] [multiplied by] [h.sup.-1], respectively, P [is less than] 0.01). Gluconeogenesis from alanine was significantly higher in WL than in WS and control subjects (0.47 [+ or -] 0.04 compared with 0.31 [+ or -] 0.04 and 0.29 [+ or -] 0.04 mmol [multiplied by] [kg.sup.-1] [multiplied by] [h.sup.-1], respectively, P [is less than] 0.01). The degree of weight loss was positively correlated with glucose and alanine turnover and with gluconeogenesis from alanine (r = 0.45 for all, P [is less than] 0.01). Conclusions: Aberrant glucose and alanine metabolism occurred in WL lung cancer patients. These changes were related to the degree of weight loss and not to the presence of lung cancer per se. Am J Clin Nutr 2000;71:583-9. KEY WORDS Weight loss, gluconeogenesis, alanine, lung cancer, stable isotope tracer, humans, liver, glucose metabolism, alanine metabolism, cachexia