Hypothalamic–pituitary–adrenal (HPA) axis control may be impaired in type 2 diabetes (T2DM). Glucocorticoids increase consumption of low quality foods high in calories, sugar, and fat. We explored ...the relationship between cortisol levels, poor blood glucose control, and food quality choice in T2DM. Twenty-seven healthy controls were age-, gender- and education-matched to 27 T2DM participants. Standard clinical blood tests and cortisol values were measured from fasting blood samples. Participants recorded all consumed food and drink items in a consecutive 3-day food diary. Diaries were analyzed for “high quality” and “low quality” foods using a standardized method with high reliability (0.97 and 0.86, respectively). Controlling for education, body mass index (BMI) and hemoglobin A1C (HbA1C), log-transformed cortisol (LogC) predicted the percent of low quality foods (
R
2
= 0.092, β = 0.360,
P
< 0.05), but not the percent of high quality foods chosen. Controlling for education, BMI, and LogC, HbA1C significantly predicted both the percent of low quality foods (Δ
R
2
= 0.079, β = 0.348,
P
= 0.024) and high quality foods chosen (Δ
R
2
= 0.085, β = −0.362,
P
= 0.022). The relationship between HbA1C and low quality food choice may be mediated by cortisol, controlling for BMI and education (
P
< 0.01). HbA1C displayed both an indirect (cortisol-mediated) effect (
P
< 0.05) and direct effect on low quality food choice (
P
< 0.05). The relationship between HbA1C and low quality food choice may be partially mediated by cortisol. Poor blood glucose control may cause HPA axis disruption, increased consumption of low quality foods.
To ascertain whether the associations between obesity, inflammation, and insulin resistance established in human adult studies are found among adolescents.
We contrasted 36 obese and 24 lean youth on ...fasting glucose, insulin levels, lipid profile, hemoglobin A1C, markers of hepatic function, white blood cell count, C-reactive protein (CRP) and fibrinogen levels. The cytokines IL-6, TNF-α, IFN-γ, IL-10 and IL-4 and the adipokines leptin, resistin, and adiponectin were also compared between the two groups. The fasting glucose and insulin values were used to estimate the degree of insulin resistance with the homeostatic model assessment of insulin resistance (HOMA-IR). T-tests and correlations were run to examine group differences and associations between groups. In addition, regression analyses were used to ascertain whether the markers of inflammation were predictive of the degree of insulin resistance.
Although obese adolescents had clear evidence of insulin resistance, only CRP, fibrinogen and leptin were elevated; there were no group differences in pro- or anti-inflammatory cytokines nor adiponectin and resistin. Anthropometric measures of obesity and level of insulin resistance were highly correlated to the acute phase reactants CRP and fibrinogen; however, the degree of insulin resistance was not predicted by the pro- or anti-inflammatory cytokine markers. Obese adolescents had higher white blood cell counts. In addition they had higher circulating alanine aminotransferase concentrations and lower circulating albumin and total protein than lean adolescents, possibly as a result of hepatocyte damage from fatty liver.
Unlike rodent or adult studies, we found that wide-spread systemic inflammation is not necessarily associated with insulin resistance among adolescents. This finding does not support the current paradigm that the associations between obesity and insulin resistance are, to a significant degree, mediated by low grade systemic inflammation. These data support the need for further adolescent studies to explore these associations.
The hypothalamus is important in hunger and metabolism. Although a lot is known about the basic role of the human hypothalamus, less is known about how the in vivo volume is affected in obesity, ...particularly among adolescents. Based on pediatric body mass index percentiles, 95 participants were assigned to lean or obese groups. All subjects had medical evaluations, including fasting blood tests, to assess insulin sensitivity and circulating CRP and neurotrophins (NGF and BDNF) and an MRI of the brain. Hypothalamic volumes were measured by a segmentation method combining manual and automated steps. Overall, obese participants had descriptively smaller hypothalamic volumes, although this difference did not reach statistical significance; however, among obese participants, females had significantly smaller hypothalamic volumes than their male counterparts. There was a significant interaction between insulin resistance and sex on hypothalamus volume; obese females with significant insulin resistance have smaller hypothalamic volumes than obese males. Obese adolescents had higher circulating CRP and neurotrophin levels. Furthermore, among obese females, BDNF concentrations were inversely associated with hypothalamus volumes (r=−0.48). Given this negative association between BDNF and hypothalamus volumes among obese insulin-resistant females, elevated neurotrophin levels may suggest an attempt at protective compensation.
The brain is the most cholesterol-rich organ in the body. Although most of the cholesterol in the brain is produced endogenously, some studies suggest that systemic cholesterol may be able to enter ...the brain. We investigated whether abnormal cholesterol profiles correlated with diffusion-tensor-imaging-based estimates of white matter microstructural integrity of lean and overweight/obese (o/o) adults. Twenty-two lean and 39 obese adults underwent magnetic resonance imaging, kept a 3-day food diary, and had a standardized assessment of fasting blood lipids. The lean group ate less cholesterol rich food than o/o although both groups ate equivalent servings of food per day. Voxelwise correlational analyses controlling for age, diabetes, and white matter hyperintensities, resulted in two significant clusters of negative associations between abnormal cholesterol profile and fractional anisotropy, located in the left and right prefrontal lobes. When the groups were split, the lean subjects showed no associations, whereas the o/o group expanded the association to three significant clusters, still in the frontal lobes. These findings suggest that cholesterol profile abnormalities may explain some of the reductions in white matter microstructural integrity that are reported in obesity.
In type II diabetes (T2DM), the hypothalamic‐pituitary axis (HPA) and cortisol regulation may be impaired. Glucocorticoids increase consumption of “comfort foods” high in sugar and fat. We explored ...the relationship between cortisol levels and food quality choice in T2DM. A total of107 middle aged individuals, 49 controls, 31 insulin resistant, and 27 with T2DM, matched on age, gender and education were evaluated. Standard clinical blood tests and cortisol values were measured from fasting blood samples. Participants recorded all consumed food and drink items in a consecutive three‐day food diary. Fruits, vegetables, fish, whole grains, and nuts were classified as high quality foods. Meat, junk food, soda, fried foods, fast food, and simple carbohydrates were classified as low quality foods. Controlling for education and waist‐to‐height‐ratio (WTHR), log‐transformed cortisol (LogC) significantly predicted the percent of low quality foods chosen (R2=.132, β=.261, P<.01) and percent of high quality foods chosen (R2=.132, β=−.261, P<.01). LogC positively correlated to Hemoglobin A1C values (HbA1C), a measure of long term glucose control (Pearson's r=.531, P<.001). Cortisol levels increase with poorer glucose control. Higher cortisol values were associated with low quality food choice while lower cortisol values were associated with high quality food choice.
Grant Funding Source: NIH grant DK064087 and NCRR grant 1UL1RR029893
The folk psychology of souls Bering, Jesse M
The Behavioral and brain sciences,
10/2006, Letnik:
29, Številka:
5
Journal Article
Recenzirano
The present article examines how people's belief in an afterlife, as well as closely related supernatural beliefs, may open an empirical backdoor to our understanding of the evolution of human social ...cognition. Recent findings and logic from the cognitive sciences contribute to a novel theory of existential psychology, one that is grounded in the tenets of Darwinian natural selection. Many of the predominant questions of existential psychology strike at the heart of cognitive science. They involve: causal attribution (why is mortal behavior represented as being causally related to one's afterlife? how are dead agents envisaged as communicating messages to the living?), moral judgment (why are certain social behaviors, i.e., transgressions, believed to have ultimate repercussions after death or to reap the punishment of disgruntled ancestors?), theory of mind (how can we know what it is "like" to be dead? what social-cognitive strategies do people use to reason about the minds of the dead?), concept acquisition (how does a common-sense dualism interact with a formalized socio-religious indoctrination in childhood? how are supernatural properties of the dead conceptualized by young minds?), and teleological reasoning (why do people so often see their lives as being designed for a purpose that must be accomplished before they perish? how do various life events affect people's interpretation of this purpose?), among others. The central thesis of the present article is that an organized cognitive "system" dedicated to forming illusory representations of (1) psychological immortality, (2) the intelligent design of the self, and (3) the symbolic meaning of natural events evolved in response to the unique selective pressures of the human social environment.
Background:
Correlative evidence indicates that apoptosis is associated with the progression of alcoholic liver disease. If apoptosis contributes to ethanol (
EtOH
)‐induced steatohepatitis and/or ...fibrosis, then mice deficient in
B
id, a key pro‐apoptotic
B
cl‐2 family member, or mice treated with a pan‐caspase inhibitor (
VX
166) should be resistant to
EtOH
‐induced liver injury.
Methods:
This hypothesis was tested in mice using a model of chronic, heavy
EtOH
‐induced liver injury, as well as in a model in which moderate
EtOH
feeding accelerated the appearance of early markers of hepatic fibrosis in response to acute carbon tetrachloride (CCl
4
) exposure.
Results:
Chronic
EtOH
feeding to mice increased
TUNEL
‐ and cytokeratin‐18‐positive cells in the liver, as well as the expression of receptor‐interacting protein kinase 3 (
RIP
3), a marker of necroptosis. In this model,
B
id−/− mice or wild‐type mice treated with
VX
166 were protected from
EtOH
‐induced apoptosis, but not
EtOH
‐induced
RIP
3 expression. Bid deficiency or inhibition of caspase activity did not protect mice from
EtOH
‐induced increases in plasma alanine and aspartate amino transferase activity, steatosis, or
mRNA
expression of some inflammatory cytokines. Moderate
EtOH
feeding to mice enhanced the response of mice to acute CCl
4
exposure, resulting in increased expression of α‐smooth muscle actin and accumulation of extracellular matrix protein.
VX
166‐treatment attenuated
EtOH
‐mediated acceleration of these early indicators of CCl
4
‐induced hepatic fibrosis, decreasing the expression of α‐smooth muscle actin, and the accumulation of extracellular matrix protein.
Conclusions:
EtOH‐induced apoptosis of hepatocytes was mediated by
B
id. Apoptosis played a critical role in the accelerating the appearance of early markers of CCl
4
‐induced fibrosis by moderate
EtOH
but did not contribute to
EtOH
‐induced hepatocyte injury, steatosis, or expression of
mRNA
for some inflammatory cytokines.
Innate immunity in alcoholic liver disease BIN GAO; SEKI, Ekihiro; BRENNER, David A ...
American journal of physiology: Gastrointestinal and liver physiology,
2011, Letnik:
63, Številka:
4
Journal Article
PDF
