Decreased expression of adipogenic genes in obese subjects with type 2 diabetes

Objective: Our objective was to delineate the potential role of adipogenesis in insulin resistance and type 2 diabetes. Obesity is characterized by an increase in adipose tissue mass resulting from enlargement of existing fat cells (hypertrophy) and/or from increased number of adipocytes (hyperplasia). The inability of the adipose tissue to recruit new fat cells may cause ectopic fat deposition and insulin resistance.r />r />Research Methods and Procedures: We examined the expression of candidate genes involved in adipocyte proliferation and/or differentiation [ CCAAT/enhancer-binding protein (C/EBP) alpha, C/EBPdelta, GATA domain-binding protein 3 (GATA3), C/EBPbeta, peroxisome proliferator-activated receptor (PPAR) gamma2, signal transducer and activator of transcription 5A (STAT5A), Wnt-10b, tumor necrosis factor alpha, sterol regulatory element-binding protein 1c (SREBP1c), 11 beta-hydroxysteroid dehydrogenase, PPARG angiopoietin-related protein (PGAR), insulin-like growth factor 1, PPARitalic gamma coactivator 1alpha, PPARitalic gamma coactivator 1beta, and PPARdelta] in subcutaneous adipose tissue from 42 obese individuals with type 2 diabetes and 25 non-diabetic subjects matched for age and obesity.r />r />Results: Insulin sensitivity was measured by a 3-hour 80 mU/m2 per minute hyperinsulinemic glucose clamp (100 mg/dL). As expected, subjects with type 2 diabetes had lower glucose disposal (4.9 plusminus 1.9 vs. 7.5 plusminus 2.8 mg/min per kilogram fat-free mass; p < 0.001) and larger fat cells (0.90 plusminus 0.26 vs. 0.78 plusminus 0.17 mum; p = 0.04) as compared with obese control subjects. Three genes (SREBP1c, p < 0.01; STAT5A, p = 0.02; and PPARitalic gamma2, p = 0.02) had significantly lower expression in obese type 2 diabetics, whereas C/EBPbeta only tended to be lower (p = 0.07).r />r />Discussion: This cross-sectional study supports the hypothesis that impaired expression of adipogenic genes may result in impaired adipogenesis, potentially leading to larger fat cells in subcutaneous adipose tissue and insulin resistance.r />

Regulation of skeletal muscle oxidative capacity and insulin signaling by the Mitochondrial Rhomboid Protease PARL

Type 2 diabetes mellitus (T2DM) and aging are characterized by insulin resistance and impaired mitochondrial energetics. In lower organisms, remodeling by the protease pcp1 (PARL ortholog) maintains the function and lifecycle of mitochondria. We examined whether variation in PARL protein content is associated with mitochondrial abnormalities and insulin resistance. PARL mRNA and mitochondrial mass were both reduced in elderly subjects and in subjects with T2DM. Muscle knockdown of PARL in mice resulted in malformed mitochondrial cristae, lower mitochondrial content, decreased PGC1α protein levels, and impaired insulin signaling. Suppression of PARL protein in healthy myotubes lowered mitochondrial mass and insulin-stimulated glycogen synthesis and increased reactive oxygen species production. We propose that lower PARL expression may contribute to the mitochondrial abnormalities seen in aging and T2DM.r />

Colour change on different body regions provides thermal and signalling advantages in bearded dragon lizards

Many terrestrial ectotherms are capable of rapid colour change, yet it is unclear how these animals accommodate the multiple functions of colour, particularly camouflage, communication and thermoregulation, especially when functions require very different colours. Thermal benefits of colour change depend on an animal's absorptance of solar energy in both UV–visible (300-700 nm) and near-infrared (NIR; 700-2600 nm) wavelengths, yet colour research has focused almost exclusively on the former. Here, we show that wild-caught bearded dragon lizards (Pogona vitticeps) exhibit substantial UV–visible and NIR skin reflectance change in response to temperature for dorsal but not ventral (throat and upper chest) body regions. By contrast, lizards showed the greatest temperature-independent colour change on the beard and upper chest during social interactions and as a result of circadian colour change. Biophysical simulations of heat transfer predicted that the maximum temperature-dependent change in dorsal reflectivity could reduce the time taken to reach active body temperature by an average of 22 min per active day, saving 85 h of basking time throughout the activity season. Our results confirm that colour change may serve a thermoregulatory function, and competing thermoregulation and signalling requirements may be met by partitioning colour change to different body regions in different circumstances.

Color change for Thermoregulation versus camouflage in free-ranging lizards

Animal coloration has multiple functions including thermoregulation,camouflage, and social signaling, and the requirementsof each function may sometimes conflict. Many terrestrial ectothermsaccommodate the multiple functions of color through color change.However, the relative importance of these functions and how colorchangingspecies accommodate themwhen they do conflict are poorlyunderstood because we lack data on color change in the wild. Here, weshow that the color of individual radio-tracked bearded dragon lizards,Pogona vitticeps, correlates strongly with background color andless strongly, but significantly, with temperature. We found no evidencethat individuals simultaneously optimize camouflage and thermoregulationby choosing light backgrounds when hot or dark backgroundswhen cold. In laboratory experiments, lizards showed both UV-visible(300–700 nm) and near-infrared (700–2,100 nm) reflectance changesin response to different background and temperature treatments, consistentwith camouflage and thermoregulatory functions, respectively,but with no interaction between the two. Overall, our results suggestthat wild bearded dragons change color to improve both thermoregulationand camouflage but predominantly adjust for camouflage, suggestingthat compromising camouflage may entail a greater potentialimmediate survival cost.