Observations on pollen harvesting by brush-tongued lorikeets

1970 ◽  
Vol 18 (4) ◽  
pp. 427 ◽  
Author(s):  
DM Churchill ◽  
P Christensen
Keyword(s):  
Subcutaneous Fat ◽  
Basal Metabolism

The staple item of diet of Glossopsitta porphyrocephala is pollen. The amount of karri pollen necessary to supply the energy for one bird's basal metabolism of 8.0 kcal/day is supplied by about 500 flowers. The moist papillae on the tongue of the lorikeets enable the birds to collect the dust-like pollen. Less than 1% of the anthers grazed are ingested during the driest months of the year when there is no nectar available. Karri nectar contains sucrose, glucose, fructose, and melibiose and is collected when it flows during the wetter flowering months. It is not a substitute for pollen, which the birds continue to harvest as their source of nitrogen. At the time the birds ingest nectar they accumulate subcutaneous fat. Nectar does not reach the stomach but is held in the crop, which enlarges to accommodate it.

Site Differences in the Basal Metabolism of Subcutaneous Fat in Obese Women*

1981 ◽  
Vol 53 (5) ◽  
pp. 948-952 ◽  
Author(s):  
PETER ARNER ◽  
PETER ENGFELDT ◽  
HANS LITHELL
Keyword(s):  
Subcutaneous Fat ◽  
Basal Metabolism ◽  
Obese Women

Repeated Occurrence of Skin Necrosis Twice Following Coumarin Intake and Subsequently During Decrease of Vitamin K Dependent Coagulation Factors Associated with Cholestasis

1982 ◽  
Vol 48 (03) ◽  
pp. 245-246 ◽  
Author(s):  
V Hofmann ◽  
P G Frick
Keyword(s):  
Skin Necrosis ◽  
Oral Anticoagulants ◽  
Subcutaneous Fat ◽  
Coagulation Factors ◽  
Fat Necrosis ◽  
Subcutaneous Fat Necrosis ◽  
Skin Changes ◽  
Factors Associated ◽  
Therapeutic Anticoagulation ◽  
Coumarin Necrosis

SummaryA female patient is described who developed skin and subcutaneous fat necrosis on two occasions after intake of acenocoumarol.Several months later identical skin changes occurred during an episode of cholestasis associated with a prolongation of the prothrombin time to an extent comparable with therapeutic anticoagulation; intake of oral anticoagulants could be excluded.This association gives new insights in the pathogenetic mechanisms responsible for the so-called coumarin necrosis and indicates that it may be not due to drug toxicity or allergy.

Correlates of visceral and subcutaneous fat thickness in non-diabetic obese and morbidly obese patients

2014 ◽  
Author(s):  
Ozen Oz Gul ◽  
Murat Pekgoz ◽  
Sumeyye Gullulu ◽  
Soner Cander ◽  
Ahmet Tutuncu ◽  
...  
Keyword(s):  
Subcutaneous Fat ◽  
Morbidly Obese ◽  
Obese Patients ◽  
Subcutaneous Fat Thickness ◽  
Fat Thickness

2059-P: Higher Propensity to Store Energy in Thigh Subcutaneous Fat Associated with a Lower Risk of NDM and Better ß-Cell Function

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2059-P
Author(s):  
XUHONG HOU ◽  
PEIZHU CHEN ◽  
LI WEI ◽  
YUQIAN BAO ◽  
WEIPING JIA
Keyword(s):  
Lower Risk ◽  
Cell Function ◽  
Subcutaneous Fat

A genome-wide linkage scan for familial partial lipodystrophy susceptibility genes in a German kindreds

2007 ◽  
Vol 30 (4) ◽  
pp. 86
Author(s):  
M. Lanktree ◽  
J. Robinson ◽  
J. Creider ◽  
H. Cao ◽  
D. Carter ◽  
...  
Keyword(s):  
Subcutaneous Fat ◽  
Visceral Obesity ◽  
Fat Distribution ◽  
Dominant Negative ◽  
Molecular Forms ◽  
Partial Lipodystrophy ◽  
Genome Wide ◽  
A Genome ◽  
Familial Partial Lipodystrophy ◽  
Promoter Mutations

Background: In Dunnigan-type familial partial lipodystrophy (FPLD) patients are born with normal fat distribution, but subcutaneous fat from extremities and gluteal regions are lost during puberty. The abnormal fat distribution leads to the development of metabolic syndrome (MetS), a cluster of phenotypes including hyperglycemia, dyslipidemia, hypertension, and visceral obesity. The study of FPLD as a monogenic model of MetS may uncover genetic risk factors of the common MetS which affects ~30% of adult North Americans. Two molecular forms of FPLD have been identified including FPLD2, resulting from heterozygous mutations in the LMNA gene, and FPLD3, resulting from both heterozygous dominant negative and haploinsufficiency mutations in the PPARG gene. However, many patients with clinically diagnosed FPLD have no mutation in either LMNA or PPARG, suggesting the involvement of additional genes in FPLD etiology. Methods: Here, we report the results of an Affymetrix 10K GeneChip microarray genome-wide linkage analysis study of a German kindred displaying the FPLD phenotype and no known lipodystrophy-causing mutations. Results: The investigation identified three chromosomal loci, namely 1q, 3p, and 9q, with non-parametric logarithm of odds (NPL) scores >2.7. While not meeting the criteria for genome-wide significance, it is interesting to note that the 1q and 3p peaks contain the LMNA and PPARG genes respectively. Conclusions: Three possible conclusions can be drawn from these results: 1) the peaks identified are spurious findings, 2) additional genes physically close to LMNA, PPARG, or within 9q, are involved in FPLD etiology, or 3) alternative disease causing mechanisms not identified by standard exon sequencing approaches, such as promoter mutations, alternative splicing, or epigenetics, are also responsible for FPLD.

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